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Role of the posterior parietal cortex in multimodal spatial behaviours Kwan, Teresa 1994

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ROLE OF THE POSTERIOR PARIETAL CORTEX IN MULTIMODAL SPATIAL BEHAVIOURS by TERESA KWAN B.Sc, The University of British Columbia, 1992  A THESIS SUBMITTED IN PARTIAL FULFILLMENT OF THE REQUIREMENTS FOR THE DEGREE OF MASTER OF ARTS  in THE FACULTY OF GRADUATE STUDIES (Department of Psychology)  We accept this thesis as conforming /io)the required standard  THE UNIVERSITY OF BRITISH COLUMBIA July 1994 © Teresa Kwan, 1994  In presenting this thesis  in  degree at the University of  partial fulfilment  of  the  requirements  for an advanced  British Columbia, I agree that the Library shall make it  freely available for reference and study. I further agree that permission for extensive copying of this thesis for scholarly purposes may be granted by the head of department  or  by  his  or  her  representatives.  It  is  understood  that  copying  my or  publication of this thesis for financial gain shall not be allowed without my written permission.  (Signature)  Department of  Psychology  The University of British Columbia Vancouver, Canada Date  DE-6 (2/88)  JULY 28, 1994  11  ABSTRACT The posterior parietal cortex (PPC) is a cortical region receiving inputs from different sensory modalities which has been shown to subserve a visuospatial function. The potential contribution of PPC in audiospatial behaviours and recognition of amodal spatial correspondences were postulated and assessed in the present study. Adult male LongEvans rats received PPC lesions by aspiration, and they were compared to sham operated control rats on three behavioural tasks. In the Morris water maze, the rats had to learn to use the distal visual cues to locate an escape platform hidden in the pool. In an open field task, the rats were assessed on their reactions to a spatial relocation of a visual or an auditory object. In a spatial cross-modal transfer (CMT) task (Tees & Buhrmann, 1989), rats were trained to respond to light signals using spatial rules, and were then subjected to transfer tests using comparable sound signals. Results from the Morris water maze, the open field, and the initial training phase of the spatial CMT task confirmed a visuospatial deficit in PPC lesioned rats. However, if given sufficient training, PPC lesioned rats could learn the location of a hidden platform in the Morris water maze, and they could also acquire spatial rules in the CMT task. Such results indicated that the visuospatial deficits in PPC lesioned rats were less severe than previously thought. On the other hand, a persistent navigational difficulty characterized by a looping pattern of movement was observed in the PPC lesioned rats in the Morris water maze. Results from the open field indicated that PPC was less involved in audiospatial behaviours. Moreover, results also indicated that PPC was not necessary for spatial CMT. Hence, data from the present study did not support the idea that PPC played an essential role in supramodal spatial abilities in the rats. Instead, data from the spatial CMT task seemed to imply a role of PPC in managing conflicting spatial information coming from different sensory modalities.  iii TABLE OF CONTENTS Abstract  ii  Table of Contents  iii  List of Tables  v  List of Figures  vi  Acknowledgement  vii  Introduction A Model of Spatial Representation Anatomy of the Posterior Parietal Cortex Behavioural Tasks Employed in the Study of Visuospatial Skills in the Rat Role of the Posterior Parietal Cortex in Auditory Spatial Behaviours Role of the Posterior Parietal Cortex in Cross-Modal Transfer Purpose of the Present Study  1 2 6 12 16 21 25  Experiment 1: Morris Water Maze Method Subjects Apparatus Procedure Results Anatomical Behavioural Escape Latency Quadrant Stay Heading Error Search Strategy  26 26 26 27 28 30 30 30 30 30 34 37  Experiment 2: Open Field Method Subjects Apparatus Procedure Results Anatomical Behavioural Locomotor Activity Contact Time for Nondisplaced Objects Visual Phase Contact Time Auditory Phase Contact Time  37 37 37 38 38 41 41 41 41 43 43 43  iv Experiment 3: Cross-Modal Transfer Method Subjects Apparatus Procedure Results Behavioural Initial Training Using Light First CMT Day Using Sound & New Rule CMT Training Using Sound & New Rule Final Test Using Light & Original Rule  46 46 46 46 47 50 50 50 52 52 52  Discussion Morris Water Maze Open Field Cross-Modal Transfer Summary  53 53 57 62 67  References  69  V  LIST OF TABLES Table 1. The number of PPC lesioned and control rats employing each search strategy on the trials before and after platform relocation in the Morris water maze  36  vi LIST OF FIGURES Figure 1. Subdivisions of the posterior parietal cortex in rhesus monkey and human Figure 2. The cytoarchitectonic regions of the cerebral cortex in the rat  8 10  Figure 3. Inputs from the primary and the secondary sensory cortices to the posterior parietal cortex in the rat  11  Figure 4. The starting locations and the platform locations in the Morris water maze.. .29 Figure 5. Representation of the posterior parietal cortex lesion in an averaged rat in the present study Figure 6. The escape latencies of PPC lesioned and control rats over the 14 trial blocks in the Morris water maze  31 32  Figure 7. The percentage of time the rats spent in each quadrant of the Morris water maze 33 Figure 8. The heading errors of PPC lesioned and control rats over the 14 trial blocks in the Morris water maze Figure 9. The testing procedure in the open field Figure 10. Locomotor activity of PPC lesioned and control rats over the six sessions in the open field Figure 11. The contact time for the displaced object for PPC lesioned and control rats over the six sessions in the open field  35 40  42 44  Figure 12. The reactions of PPC lesioned and control rats towards the spatial change in the visual and the auditory phases  45  Figure 13. The experimental design of the spatial cross-modal transfer task  49  Figure 14. Performance of PPC lesioned and control rats on the spatial cross-modal transfer task  51  Vll  ACKNOWLEDGEMENT I would like to thank the Natural Sciences and Engineering Research Council of Canada and the University of British Columbia for awarding me graduate scholarships. I would also like to thank all the students who have helped me with the behavioural testings in the past two years: Nicole Culos, Jennifer Dang, Nancy Dwornick, James Ho, Derek Hong, Todd Lannard, Fay Leong, Scott Leong, Leung Man, Colin McEown, Sarah Wasty, and Cecilia Wong. Moreover, I would especially like to thank Christopher Yong for making the equipment work so well and Lucille Hoover for helping me in so many ways. The help provided by all these wonderful people will always be remembered. Most importantly, I would like to thank Richard Tees for being my supervisor and for teaching me so much.  1  INTRODUCTION One widely held belief about the visual system is that it is divided into separate pathways which are responsible for processing different aspects of our visual world. For example, Mishkin, Ungerleider, and Macko (1983) have proposed that the visual system consists of two pathways. One pathway (the ventral pathway), which interconnects the striate (primary visual), the prestriate (secondary visual), and the inferior temporal cortices, is responsible for the visual identification of objects. Another pathway (the dorsal pathway), which interconnects the striate, the prestriate, and the posterior parietal cortices, is responsible for the visual location of objects. It is believed that the ventral pathway is composed of further subdivisions, and that these subdivisions are responsible for analysing different physical properties of a visual object such as its size, shape, colour, and texture. The results from such analyses are integrated at the inferior temporal cortex, the final "target" of the ventral pathway, to form a complete percept of the visual identity of the object (Zeki, 1978). While this view regarding the functioning of the ventral pathway has been accepted by some researchers, there have been few comprehensive hypotheses proposed to describe the processes of the dorsal pathway. Moreover, many believe that the dorsal pathway may be a more complicated system than the ventral pathway. The dorsal pathway may be processing spatial information from sensory modalities other than vision because the posterior parietal cortex also receives inputs from other sensory modalities (Stein, 1991). Moreover, spatial perception is believed to be a supramodal ability (Semmes, 1967). Hence, studies on the dorsal pathway and its critical "targets" should diverge from simply focusing on the visual modality to including other sensory modalities. For the above reason, the present study was done with the intention to provide more data about the functions of the posterior parietal cortex (PPC), the final "target" of the dorsal pathway. A model of spatial representation is first presented and discussed as background materials for the study of the neural basis of spatial behaviours. Then, a brief  2  description of the anatomy of PPC is provided. In the ensuring sections, some key studies on the spatial functions of PPC are examined in detail, and the rationale for the present study is presented. A Model of Spatial Representation Many studies of the PPC seem to have focused on its potential role in visuospatial behaviours. Nevertheless, very few comprehensive ideas have been offered on the exact nature of spatial perception itself and its neural representations. However, Kolb and Whishaw (1990) have proposed a model of spatial representation, in which PPC plays a major role. According to this model, a coordinate system is set up in PPC to represent the external space, and objects in space are located in this coordinate system. In addition, PPC is also responsible for directing movement in regard to stimuli in space. While PPC contains the location information for an object, the inferior temporal cortex (ITC) serves to identify the object by its visual features. Both PPC and ITC send projections to the hippocampus (HC) and the frontal cortex (FC). Information from PPC and ITC are combined in HC to form a representation which contains both the location and the identity of the object. Then, HC is viewed as essential in ensuring this representation goes into long-term storage elsewhere in the cerebral cortex. Finally, FC is described as serving to direct movements to targets in space by using the stored information. There is a great deal of evidence in support of the differential roles of PPC and ITC. For example, Pohl (1973) found that lesion to ITC but not to PPC in monkeys produced an impairment on the object discrimination task, a task in which the monkeys had to discriminate and choose one of two different objects based on its visual features in order to receive a food reward. On the other hand, lesion to PPC but not to ITC resulted in deficits on the landmark task, also a two-choice discrimination task but where the correct choice of the object was based on its spatial proximity to a third object. McDaniel and Thomas (1978) also discovered a similar functional dissociation between the two brain structures using rats and slightly different behavioural tasks. Even when complex visual  3  patterns were used, McDaniel, Wildman, and Spears (1979) found that PPC lesioned rats were still as unimpaired on the visual discrimination task as unoperated rats, whereas ITC lesioned rats were significantly impaired. A functional dissociation between PPC and ITC was also found by Kolb, Buhrmann, and McDonald (1989). Moreover, their study also revealed functional differences of these two structures with FC, another component of the neural model of spatial representation. In their study, rats with lesion of PPC or FC were impaired on a spatial navigation task which required the use of distal cues. However, only FC lesioned rats were also impaired on a navigation task which required the use of bodycentered spatial skills. On the other hand, ITC lesioned rats had no deficit on any of the navigation tasks, but they had difficulties in a test of visual recognition memory. Thus, results from most studies do seem to support the separate roles of PPC and ITC as outlined in the model. The data regarding FC are less conclusive. According to the model, both PPC and FC are responsible for directing movements to targets in space. However, the model is not clear if the two structures are responsible for different types of movements, using different spatial information and memory processes. In fact, some researchers could not find a difference between the two structures. For example, Lawler and Cowey (1987) found that both PPC and FC lesioned monkeys were impaired, compared to ITC lesioned monkeys, when required to use the colour of a spatially remote cue to locate a food reward. Also, Thomas and Weir (1975) found that both PPC and FC lesioned rats were equally impaired on Lashley's Maze III, a task which required the rat to find its way through a system of interconnecting alleys to get from a startbox to a goalbox. Despite the failure of some researchers in differentiating PPC and FC, others have found a functional dissociation between PPC and FC. Kesner, Farnsworth, and DiMattia (1989) tested rats on two tasks intended to tackle separate spatial navigation processes. A cheese board task was employed to test allocentric navigation and an adjacent arm radial maze task was used to evaluate egocentric navigation. They found that PPC was responsible for allocentric navigation, involving  4  spatial behaviours in which the relations between places that are independent of one's body orientation in space are needed. Such findings are certainly consistent with the spatial coordinate system of PPC as described in the model by Kolb and Whishaw (1990). On the other hand, FC was responsible for egocentric navigation, in which responses are dependent on the accurate assessment of one's body orientation in space. Using different behavioural tasks, Kolb, Sutherland, and Whishaw (1983) had also found different spatial deficits in PPC and FC lesioned rats; however, their results did not support the dissociation into allocentric and egocentric spatial behaviours. They found that FC lesioned rats were significantly impaired in the Morris water maze and the radial arm maze, both of which served to test allocentric navigation, but these rats were not impaired in the Grice box, in which the use of egocentric navigation was required. On the other hand, PPC lesioned rats were relatively unimpaired in the allocentric tasks, but they were significantly impaired on the egocentric task. Kesner, DiMattia, and Crutcher (1987), with a different focus on spatial behaviours, also found a difference between the two structures. In their study, a radial arm maze was used, and some of the arms of the maze were chosen to be baited on every trial. Two types of spatial memory were tested: reference memory (or long-term memory) was indicated by the ability of the rat to remember the baited arms over days, and working memory (or short-term memory) was assessed by the ability of the rat to avoid re-entry errors to already visited arms on a trial. The results showed that PPC lesioned rats had a deficit on reference memory only, whereas FC lesioned rats had deficits on both types of memory. Hence, results from some studies do support a difference in the spatial functions of PPC and FC, but the exact nature of this difference is still uncertain. It seems that researchers attempting to differentiate the spatial roles of PPC and HC have been equally unsuccessful. For example, Kesner (1993) found that FC lesioned rats could not learn to associate different food cues to different spatial locations on a radial arm maze, but both PPC and HC lesioned rats could learn the association. On the other hand, DiMattia and Kesner (1988b) did find a difference between PPC and HC.  5  They found that both PPC and HC lesioned rats were impaired in locating a hidden platform in the Morris water maze, but HC lesioned rats were less impaired than PPC lesioned rats, and HC lesioned rats could adopt a looping strategy to allow rapid location of the platform. Most importantly, it was found that presurgical training on the task facilitated performance of the HC as well as the PPC lesioned rats. This result seems to be consistent with a proposition of the model in that the long-term store of the representation(s) of objects and their location exists in parts of the cerebral cortex but not the HC, while the HC is essential in the formation of new representations. Additional support regarding the transient role of HC has been provided by Kametani and Kesner (1989) using the radial arm maze to assess reference and working memories. Their results indicated that PPC was necessary in the case of reference memory, whereas HC was necessary in the case of working memory. Finally, Thompson and Yu (1985) compared the effects of lesions to each component identified in the model. In their study, weanling rats received lesions to one of the four brain structures, and were then tested on three tasks: visual discrimination, maze learning (a spatial task), and inclined-plane discrimination (a vestibular-proprioceptivekinesthetic discrimination). No functional dissociation between PPC and ITC was found: both PPC and ITC lesioned rats were impaired on visual discrimination and maze learning. Moreover, PPC lesioned rats were also impaired on the inclined-plane task. FC lesioned rats had no deficit on any of the three tasks, and HC lesioned rats had deficit in maze learning only. However, care should be taken in interpreting their findings. Other researchers have since shown that the PPC lesion in neonatal rats produces much larger anatomical and behavioural effects than a similar lesion in adulthood (Kolb, Holmes, & Whishaw, 1987). In summary, results from most lesion studies seem to confirm the functional dissociation of PPC and ITC into spatial localization and visual identification, respectively. However, results regarding the effects of lesions to other structures are less conclusive.  6  For example, some investigators found that there was no difference between the spatial functions of PPC and FC, whereas other researchers found that PPC was responsible for allocentric navigation and FC was responsible for egocentric navigation. Results regarding HC lesioned subjects also ranged from having no spatial deficit to having slight deficit. However, there seem to be some positive evidence supporting the idea that HC is responsible only for the formation of new representations of objects, with long-term storage of the representations carried out by other cortical sites. The largely inconclusive results may be due to the fact that most of these studies were not designed to evaluate the model, so the behavioural tasks employed may not be appropriate for drawing a conclusion regarding the model. Also, the model seems tentative and may require elaboration of the different proposed functions of the different structures. In any case, the model is useful in providing a framework in studying and understanding the different brain structures involved in spatial behaviours. Most importantly, in the study of the spatial functions of PPC, it should be remembered that PPC may not be the only neural structure responsible for spatial behaviours. Anatomy of the Posterior Parietal Cortex The cerebral cortex can be divided into different regions according to their functions, neural connections, or even cellular characteristics. Perhaps the most precise way to locate these regions is by using their different cellular characteristics. Some examples of the cellular characteristics (or cytoarchitecture) frequently used by researchers are cell type, cell size, and cell density. Despite the precision, different researchers sometimes do disagree on the exact locations, and differences between the cytoarchitectonic classifications used by different researchers do exist. Based on Brodmann's cytoarchitectonic classification, the parietal lobe of the cerebral cortex is divided into several areas: Brodmann's areas 1, 2, 3, 5, 7, 39, 40, and 43. Studies relating these areas with behavioural data have discovered that these areas constitute three functional zones. The first zone contains areas 1, 2, 3, 43 and portions of area 5. This  7  anterior zone is the location of the primary and the secondary somatosensory cortices, which are responsible for the basic sensation of touch. The other two zones contain areas 7, 39, 40, and portions of area 5. These two posterior zones are referred to as the posterior parietal cortex (PPC), the region postulated to have a multimodal spatial function. One disadvantage of Brodmann's classification is that the areas are slightly different across species. On the other hand, von Economo's cytoarchitectonic system is more consistent across species. Based on von Economo's system, the PPC areas are as follows: Brodmann's areas 5 and 7 are referred to as a single area PE, area 39 is called area PG, and area 40 becomes area PF. Using von Economo's classification, researchers have located further subdivisions of PPC. In the rhesus monkey, nine major subdivisions of PPC have been identified: PE, PEa, PEc, PF, PFG, PG, PGm, POa, and Opt (Pandya & Yeterian, 1985). Moreover, a highly similar description of the subdivisions of the human PPC has also been made by a separate group of researchers (Eidelbery & Galaburda, 1984). For a comparison of the subdivisions of PPC in monkey and human, see Figure 1. Perhaps the most significant characteristic of the PPC is its connections with other neural structures. Many modalities of sensory information converge in PPC. For example, Stein (1991) has summarized the cortical inputs to PPC in the monkey. According to this summary, PPC receives two different streams of visual information, one from the primary visual cortex by way of the secondary visual cortex (the dorsal pathway of Mishkin et al., 1983), and the other from the superior colliculus by way of the pulvinar (this stream carries oculomotor information as well). Auditory inputs reach PPC through the tempo-parietal area, a higher order auditory area. Somatosensory information, touch, position, and vibration senses are relayed through the primary somatosensory cortical areas to PPC. Finally, vestibular inputs also enter PPC by way of the vestibular cortex, which is situated postero-laterally to the somatosensory cortex. In short, PPC receives inputs from the visual, auditory, somatosensory, and vestibular systems. Moreover, it also  8  Figure 1. Subdivisions of the posterior parietal cortex in rhesus monkey (top) and human (bottom). (From Kolb & Whishaw, 1990).  PGm  OPE  OPG  PFG  OPH  9  receives motivational signals from the limbic system. In return, PPC provides outputs to motor centres in the basal ganglia, frontal eye fields (medial frontal cortex), superior colliculi, and cerebellum. Kolb and Whishaw (1990) have also outlined five types of projections from PPC. The first type of projection largely originates from the PPC areas of PE, PEc, and PGm, and it terminates in the secondary motor cortex. The second type projects from areas PF, PFG, and PG to the frontal cortex. The third type projects from area Opt to the hippocampus. The fourth type connects area PG with the temporal lobe. Finally, the fifth type of projection goes from area PG to the cingulate cortex. Despite the identification of these projection systems, the exact functions of these systems remain uncertain. Although little is known about the cortical connections in the human brain, it is believed to have great similarities with that of the monkey. This conclusion is largely based on the similarities of the cytoarchitectonic subdivisions of the PPC between the two species. However, it is necessary to note that there are still differences between the monkey and the human PPC. For example, the overall size of the human PPC is larger than that of the monkey, and there may be more subdivisions in the human. Moreover, there is evidence of asymmetry in the human PPC, but not in that of the monkey. Despite the differences between the human and the monkey PPC, researchers do not think that the differences are significant enough to render comparison between the two species impossible (Kolb & Whishaw, 1990). Most importantly, based on various anatomical criteria such as cytoarchitecture and cortico-cortical connections, Kolb (1990) has concluded that the rat PPC is a useful analog of the monkey PPC (Figure 2). One major difference between the rat and the monkey is that in the rat, PPC receives inputs directly from the primary sensory cortices, instead of through the secondary sensory cortices as in the monkey (Figure 3). However, this difference may simply reflect a less advanced development of the secondary sensory cortices in the rat. In other words, there seem to be enough anatomical similarities of PPC across a variety of species including the rat, the  10  Figure 2. The cytoarchitectonic regions of the cerebral cortex in the rat. The posterior parietal cortex is labeled as PPC in the lateral (top) and dorsal (bottom) views. (FromZiUes, 1990).  11  3. Inputs from the primary and the secondary sensory cortices to the posterior parietal cortex (PPC) in the rat. Ocl = primary visual cortex; Oc2L, Oc2M = secondary visual cortex; Te2 = inferior temporal cortex; Pari = primary somatosensory cortex; Par2 = secondary somatosensory cortex; Tel = primary auditory cortex; and Te3 = secondary auditory cortex. (From Kolb, 1990).  Ocl  PPC Pari  Te3  Tel  12  monkey, and the human to allow comparison of behavioural data from studies using these species. The aggregated knowledge from such data should certainly facilitate our understanding of the functions of PPC. Behavioural Tasks Employed in the Study of Visuospatial Skills in the Rat Spatial deficits can be manifested in a variety of ways. For example, the deficit can be an allocentric and/or an egocentric one. Long-term spatial memory can be disrupted while short-term spatial memory is spared. Moreover, a representation of the topographical relationship among objects explored could be formed and be intact in the brain, while the subject's performance could be deficient due to a failure to direct appropriate responses at testing. Usually, a careful choice of the behavioural task can serve to clarify the exact nature of any deficit. For this reason, a number of behavioural tasks have been designed to test spatial behaviours in the rat as well as in other species. Some of these behavioural tasks employed by researchers to study spatial behaviours in rats have been briefly described in a previous section. A more detailed discussion of a few of the tasks is provided below. Some classic tasks which have been employed to study spatial behaviours in the rat are the Lashley III maze and the Hebb-Williams maze. These two mazes both consist of a closed field being divided into a number of interconnecting alleys. In order to successfully complete the task, the rat has to navigate through the alleys to get from a startbox to a goalbox. Early studies employing these mazes had shown that PPC lesioned rats were impaired on both the Lashley III maze (Thomas & Weir, 1975) and the Hebb-Williams maze (Boyd & Thomas, 1977), compared to control rats. One major disadvantage of such mazes is that they revealed little about the exact nature of the spatial deficits, especially in dissociating allocentric from egocentric deficits. Another task which had been shown sensitive to PPC lesion was the spatial reversal task (McDaniel & Thomas, 1978). This task has the advantage that it specifically tested egocentric navigation. The apparatus employed in this task is called the Grice box by some researchers (Kolb & Whishaw,  13  1990). It consists of a startbox which opens into an area where the rat must choose between two parallel alleys. The rat is trained to go into only one of the alleys, on its right or left side, in order to receive a food reward. Once the rat has achieved criterion performance on an alley, the other alley becomes the correct choice. The spatial reversal task usually involves several reversals of alleys designated as the correct choice. While the Lashley III maze, the Hebb-Williams maze, and the Grice box have been used to run only a specific task, the radial arm maze has been employed by many researchers to assess different manifestations of spatial deficits in a variety of behavioural tasks. The typical radial arm maze contains a central platform, with a number of arms radiating from the platform like spokes in a wheel. Sometimes a door is installed between the platform and each arm, and this door can be opened or closed by the experimenter. Two classic spatial tasks which employed the radial arm maze are the win-shift task and the win-stay task. In both, the rat is initially exposed to a series of trials; and on each trial, an arm is baited and opened. Only a subset of arms are opened during these trials. In the test phase, the rat is confronted with the same maze with only two opened arms. In both tasks, one of these two arms has been among the baited arms, and the other arm has been among the closed arms during the initial phase. In the win-shift task, the rat is required to choose the arm that has previously been closed; and in the win-stay task, the rat has to choose the arm that has previously been baited in order to obtain a food reward. PPC lesioned rats were shown to have difficulties on both the win-shift and the win-stay task (DiMattia & Kesner, 1988a). A similar procedure has also been used to test other kinds of behaviours. In a test of visual spatial order memory, the rat is confronted during the test phase with two arms that have previously been opened and baited. To obtain a food reward, the rat must choose the one which was opened earlier in the sequence of trials presented initially. In the test of item spatial memory, the same procedure as that for the win-shift task is used. PPC lesioned rats were not impaired on the order spatial memory task, but they were impaired on the item spatial memory task (Kesner & Gray, 1989). The  14  radial arm maze has also been used to study allocentric navigation. In this task, doors are not utilized. A subset of the arms are baited, and the rat is allowed to use distal cues to learn the locations of these baited arms which remain the same everyday. It was found that PPC lesioned rats made more errors compared to control rats (Kolb & Walkey, 1987). Another apparatus which can be used to test various abilities is the Morris water maze. The Morris water maze employed by most researchers consists of a circular pool containing water made opaque (Morris, 1981). An invisible platform is situated in the pool, and the rat is released into the water and is required to find the platform (using distal or proximal cues depending on the task) in order to escape the cold water in the pool. It has been shown that the intact rat can learn to find the platform even though the point of its release from the side of the pool has a different angular relationship to the platform on each trial. In other words, the rat can learn to use the topographical relationship among the platform and the various cues around and outside the pool to locate the platform, instead of simply making a series of head turns to reach the platform. The Morris water maze also has advantages over the land-based tasks (Sutherland & Dyck, 1984). For example, rats can usually master the Morris water maze tasks within only a few trials. Odor cues frequently acting as a confound on the land-based spatial tasks are largely eliminated by the water. Food deprivation is not necessary to motivate the rats to perform in the water. A variety of tasks involving the water maze have been used to study the effects of PPC lesion in the rats. For example, in the visible platform task, the top of the escape platform is above water level, and the platform is moved to a different location from trial to trial. PPC lesioned rats are found to be as capable as control rats in using the proximal cue to locate the platform. On the other hand, PPC lesioned rats are found to be less efficient on other tasks involving an invisible platform, such as when the top of the platform is a little below water level and is invisible to the rat in the pool. In the landmark  15  navigation task, the location of the hidden platform is marked by a visual cue attached to the wall of the pool just behind the platform, and PPC lesioned rats have been reported to be unable to learn this task, whereas unlesioned control rats do. In the place navigation task, the rats are allowed to use distal visual cues (on the walls of the testing room, etc.) to locate the hidden platform which is maintained in the same location from trial to trial. PPC lesioned rats are also found to be impaired on this task in comparison to control rats (Kolb & Walkey, 1987). Thus, these findings seemed to show that PPC was responsible for ability to utilize visual cues separated from a target in space to navigate accurately to that target. The deficits shown by PPC lesioned rats in the place navigation task in the Morris water maze are obvious from their longer escape latency compared to the control rats. Despite their longer escape latency, a gradual improvement in escape latency has been observed in the lesioned rats over trials. The issue obviously then becomes whether this improvement is due to the lesioned animals learning something about the location of the platform or to the animals simply adopting a more efficient strategy in searching the water maze. If the lesioned rats had learnt the location of the platform, moving the platform's location after many trials should disrupt their performance as it would the performance of unlesioned animals and an increase in escape latency would then be recorded. On the other hand, no such disruption would occur if the lesioned rats had simply adopted a more efficient search strategy. Results from previous studies (DiMattia & Kesner, 1988b; Kolb & Walkey, 1987) seemed to indicate that while moving the platform disrupts the performance of the control rats, such disruption has not been consistently observed in case of the PPC lesioned rats. It is possible, however, that the lesioned rats would demonstrate unequivocal learning of the location if they were given more training before the "probe" relocation of the platform. For this reason, a modification of the place navigation task was used in Experiment 1 of the present study to further investigate the extent of the spatial deficits observed in PPC lesioned rats. In this experiment, both the PPC lesioned and the  16  unlesioned control rats were allowed more training trials in the Morris water maze before the platform was relocated. Moreover, in addition to the escape latency, other behavioural measures of the rats' behaviours in the water maze were systematically recorded and analysed, including the percentage of time the rat spent in each of the four quadrants of the pool, the heading error the rat made when it was released into the pool, and the searching swim pattern the rat displayed. Analysis of these multiple behavioural measures allows a closer examination and hence a clearer understanding of the spatial deficits widely observed in PPC lesioned rats on a variety of visuospatial tasks employing different types of apparatus. Role of the Posterior Parietal Cortex in Auditory Spatial Behaviours Because PPC is a cortical region receiving sensory inputs other than visual inputs and spatial behaviour is believed by many to be a supramodal ability, it is interesting to examine if PPC also plays a role in spatial behaviours involving other sensory modalities. Unfortunately, very few systematic studies have been done to date to investigate such a possibility. One reason for this may be the fact that investigations of the somatosensory, olfactory, or vestibular signals involve problems of stimulus contact and manipulation which can be partially solved with sophisticated apparatus and techniques which are not widely available. Moreover, behavioural tasks used to study these different sensory systems within the spatial context are difficult to design. However, some researchers have overcome the difficulties and have collected some data regarding the role of PPC in audiospatial behaviours. In a study by Farah, Wong, Monheit, and Morrow (1989), human patients with right PPC damage were tested on a variant of the simple reaction time task. In this task, the patient had to focus on a visual fixation point in the centre of a screen. Visual and auditory cues located on the right or the left of the fixation point were used to signal the location of a visual target which could also be presented to either side of the fixation point. When the subject detected the target, a response key was pressed, and the reaction  17  time was recorded. On some trials, the cues were valid; whereas on other trials, cues were invalid. It was found that, on invalid trials, the patients took longer to disengage from either a visual or an auditory cue in order to attend to a visual target presented on the left side, the side believed to be affected by their unilateral lesions, compared to when the target was presented to the unaffected side. Because the visual and the auditory cues had equal effects on a visuospatial attention deficit caused by PPC lesion, the authors concluded that both the visual and the auditory systems utilized a supramodal spatial attention neural mechanism which depended on PPC. While the results of Farah et al. (1989) were consistent with this conclusion, results from another human study seem to be less conclusive. Pinek, Duhamel, Cave, and Brouchon (1989) tested patients with right or left PPC damage in a sound localization task. These patients were blindfolded, and they had to point to a sound presented to them through one of the loudspeakers along a semicircular arrangement. In general, patients with right lesions had slight auditory localization deficits in their left field, but they had persistent left visual neglect. On the other hand, patients with left lesions were severely impaired on sound localization in both hemifields, but they did not exhibit any sign of visual neglect. Thus, the results seemed to indicate that PPC (especially the left side) was responsible for audiospatial behaviours; however, the spatial role of PPC did not appear to be supramodal since PPC induced spatial deficits in the visual and the auditory modalities could be dissociated. Interestingly, Crowne, Richardson, and Dawson (1986) had found evidence in support of a supramodal spatial mechanism in rats. Rats receiving unilateral PPC lesions and assessed on their orienting responses to visual, auditory, and tactile stimuli presented to either side showed a strong contralateral neglect of all three kinds of sensory stimuli. This neglect caused by the unilateral lesions was transient and only lasted for a few weeks, but the neglect was multimodal. Although a conclusion cannot be drawn from the above studies regarding a supramodal spatial function of PPC, the evidence is consistent with a role of PPC in  18  audiospatial behaviours as well as in visuospatial behaviours, possibly with distinct involvements with the visual and the auditory systems. Obviously, more work needs to be done in order to gain a better understanding. The open field has been used to investigate visuospatial behaviours in the rat, and it would seem to be an excellent task choice to also investigate its audiospatial behaviours. In most open field studies, a large arena is used which contains a few objects at different locations. The typical test procedure involves placing the rat into the open field, and allowing the rat to explore the open field and interact freely with the objects. Next, the rat is removed from the open field, and after a delay, the rat is reintroduced into the open field. During the delay, some or all of the objects in the open field are relocated or replaced by other objects. Upon its reintroduction, the rat's reactions to the changes are assessed by comparing changes in various behavioural measures obtained before and after the change/delay. For example, some fundamental measures which have been used by researchers are contact time with the objects, locomotor activity as reflected by zone crossings, number of rearings and proppings, time engaged in sniffing, and number of groomings (Renner & Seltzer, 1991). Hence, although a variety of behaviours are usually exhibited by the rat in the open field, a systematic and objective record of these behaviours needs to be taken for proper analysis of the experimental outcomes. Perhaps the most employed behavioural measure in the study of the rat's reactions to spatial or object changes in the open field has been the object contact time. When a rat is first introduced into an open field with objects, it will spend a lot of time exploring the objects, and initial contact time is high. Over repeated sessions, the rat will habituate to the particular arrangement of objects, and the contact time will gradually decrease. When changes are made to the objects, rats can "dishabituate", and a sudden increase in contact time can be recorded. For example, some researchers have shown that moving some of the objects which resulted in a change in the geometric relation between the objects causes normal hamsters to dishabituate to all of the objects; however, if all the objects are moved  19  such that the same geometric relations are retained, the hamsters do not dishabituate (react) to such changes (Thinus-Blanc, Bouzouba, Chaix, Chapuis, Dump, & Poucet, 1987). If the overall geometric relation of the objects is preserved but the locations of some objects are interchanged, normal hamsters do increase their contact time selectively to the relocated objects (Poucet, Chapuis, Durup, & Thinus-Blanc, 1986). Finally, another behavioural measure, locomotor activity, which is usually reflected by the number of zone crossings made by the rats in the open field, has also been employed in some studies to reveal reactions to spatial change. Wilz and Bolton (1971) found that a group of normal gerbils increased their locomotor activity in response to a spatial rearrangement of the objects in an open field, whereas no such increase occurred when there was no spatial change upon reintroduction. The object contact time is a frequently employed measure as well as a sensitive measure to reveal spatial deficits in brain damaged rats. For example, Poucet (1989) showed that normal rats would dishabituate with an increase in contact time to both the displaced and the nondisplaced objects following a spatial change in the open field, frontal cortex lesioned rats would only dishabituate to the displaced objects, and septal lesioned rats would not dishabituate to any of the objects. Other investigators found that following reversible inactivation of the hippocampus using lidocaine, rats would not dishabituate to a missing stimulus object, whereas unlesioned normal rats would exhibit an increase in the time spent exploring the previous location of the object (Thinus-Blanc, Save, Poucet, & Buhot, 1991). Both contact time and locomotor activity were used in a study of spatial and nonspatial behaviours in PPC lesioned and hippocampal lesioned rats. It was found that all the rats did habituate to a spatial arrangement of objects in an open field, and this habituation was reflected by a gradual reduction in both object contact time and locomotor activity over sessions. Following a relocation of some of the objects, the unlesioned rats increased their object contact time, whereas rats with either types of lesion failed to react to the change. However, when one of the objects was replaced by a different object, both  20  lesioned and unlesioned rats showed an increase in contact time (Save, Poucet, Foreman, & Buhot, 1992). This result seemed to be consistent with findings using other behavioural tasks, which indicated that PPC played a role in the visuospatial localization but not in the visual identification of objects. Due to the successful use of the open field paradigm by Save, Poucet, Foreman, and Buhot (1992) in revealing the visuospatial deficits in PPC lesioned rats, this paradigm was adopted and extended in Experiment 2 of the present study to test both visuospatial and audiospatial behaviours. The experiment consisted of two phases, a visual and an auditory phase. The testing procedure for the visual phase was similar to that in Save, Poucet, Foreman, and Buhot (1992). Basically, the rats were allowed to explore and habituate to an arrangement of objects in the open field over a few sessions. Next, a relocation of one of the objects was made, which yielded a different geometric relation among the objects. Contact time for each object and locomotor activity were recorded in each session in order to reveal the reactions of the rats towards the spatial change. In the auditory phase of the experiment, the same objects and procedure were used. The only difference was that since the relocated object was a container with a metronome inside, the metronome was switched on during all sessions of the auditory phase. Hence, in the auditory phase, unlesioned rats could use either the visual or the auditory information to detect the spatial change. On the other hand, because PPC lesioned rats had been shown to ignore the relocation of an object in the visuospatial test, if they did react to spatial change in the auditory phase, the reaction must be a result of the additional auditory feature of the object. If PPC lesioned rats did react to change in the auditory phase, such evidence would suggest that PPC might not be involved in audiospatial behaviours. However, if the lesioned rats did not react in either phase, then evidence would be provided that PPC had a role in both visuospatial and audiospatial behaviours. It should be noted that this experiment is not a test of whether PPC is the site of a supramodal spatial mechanism or PPC is a region where spatial processes for different sensory  21  modalities co-located but remained segregated. However, the advantage of being able to use the same objects and procedure in both phases in the present experiment could be helpful in comparing audiospatial and visuospatial reactions under comparable conditions, and thus provide a more rigorous test of the spatial functions of PPC. Role of the Posterior Parietal Cortex in Cross-Modal Transfer If PPC is really the cortical region containing a supramodal spatial mechanism, then PPC lesioned subjects may also be impaired on tasks which test the subjects' ability to recognize or respond to the amodal stimulus property of location. Amodal properties are properties which remain unchanged regardless of the sensory modalities through which test materials are being presented. Some examples of amodal signal properties are space, time, number, and size. Furthermore, there are several amodal properties relating to space as described by Mendelson (1979): a point in space is called location, an interval of space is called extent, a pattern of intervals over space is form, change of pattern (rate) over space is texture, and change of rate over space is texture gradient. An understanding of these amodal properties can be demonstrated by successful performance in cross-modal transfer (CMT) tasks. CMT tasks usually involve training the subject to acquire a response rule using stimuli from one sensory modality; this initial training is followed by a transfer test of the response rule using stimuli from a different modality. An example of a display of CMT for the amodal property of location would occur when a person heard a sound at a certain point in space and looked expecting to see an object making the sound at that same location. CMT for the amodal property of time could be demonstrated by a person's improved accuracy in timing sound signals after practising on timing light signals. CMT abilities are also reflected in our language, many adjectives can be applied to stimuli from more than one modality. For example, adjectives of duration such as "brief and "long" can be used to describe either light or sound signals. Based on the multimodal inputs to PPC, different researchers have suggested that PPC might be responsible for CMT for a variety of amodal properties (Kolb & Whishaw,  22  1990; Stein, 1991). Indeed, studies of parietal lobe damaged human patients have revealed that both the right and the left parietal lobes are involved in certain types of CMT. It was found that patients with either right or left parietal damage were impaired on an auditory-visual matching task, in which they were required to choose a visual dot pattern that corresponded to the auditory pattern tapped by the experimenter. On the other hand, left but not right parietal damage patients were impaired on the visual-tactile and the tactile-visual matching tasks, in which they had to form a match between a visual pattern that they saw and a raised wire pattern that they felt by hand (Butters & Brody, 1968; Butters, Barton, & Brody, 1970). Despite the positive results from studies of human patients, studies using monkeys as subjects seem to indicate otherwise. Streicher and Ettlinger (1987) trained monkeys to perform visual-tactile and tactile-visual matchings of a large number of different junk objects. These monkeys then received lesions to PPC and two other cortical sites which the researchers postulated to have a role in CMT (the frontal and the temporal cortices). These lesions were performed either in one stage or successively. Postoperative performance indicated that the monkeys with even the most extensive cortical lesions were either unimpaired or only slightly impaired in retaining the matching tasks. On the other hand, Wilson and Wilson (1962) found that unlesioned monkeys, which had received previous training on tactile object discriminations, were facilitated later in respect to visual object discriminations. However, PPC lesioned monkeys did not appear to benefit from such previous training. Although this result seemed to indicate that PPC was responsible for intersensory facilitation of object discrimination learning, it did not really involve a test of cross-modal matching. More studies must be done in order to get a more definite answer regarding the role of PPC in CMT Often, lesion studies using rats can serve to clarify uncertainties arising from human case studies since the experimenters can choose to make precise lesions in the rats. Despite such an advantage, rats have not been widely used in CMT studies. Most  23  researchers seem to believe that CMT tasks are difficult, and that even normal unoperated rats would not be able to learn to perform such tasks. However, despite this skepticism, CMT for several amodal attributes such as intensity, time, and space has been demonstrated in normal rats. For example, Over and Mackintosh (1969) trained rats to lever press for food following a light signal of one intensity, but to inhibit responding following a light signal of another intensity. Once the rats had acquired this task, they were tested using two different intensities of sound. It was found that rats which were trained to respond to the more intense light would respond to the more intense sound, whereas those trained to respond to the less intense light would respond to the less intense sound. Moreover, a similar transfer was observed when the rats were first trained with sound and tested with light later. Indeed, using this paradigm, researchers have found some evidence that PPC was involved in CMT of intensity (Yeterian, Waters, & Wilson, 1976). Other than CMT of intensity, normal rats can also perform CMT of time. Roberts (1982) trained rats to lever press for food 40 seconds after the presentation of a light or a sound signal. Next, he trained the rats to respond 20 seconds after the presentation of the light signal. It was found that the rats would demonstrate peak response at 20 seconds after presentation of the sound signal. Thus, the rats would use the new rule with the sound signal even though no new training was given with respect to the sound signal. Successful transfer was also found when the second training was given with respect to the sound signal and the transfer was to the light signal. Using a similar temporal generalization procedure, Meek and Church (1982) trained rats to discriminate three durations of light signals. For one group of rats, the durations of the light signals were 2, 4, and 6 seconds; and for the other group of rats, the durations were 6, 12, and 18 seconds. For both groups, response to only the intermediate duration would result in food reinforcement. Once the rats had learnt this discrimination, sound signals of the same durations were used instead of the light signals. It was found that rats from both groups  24  would continue to respond maximally to the sound signal with the intermediate duration. Using a choice discrimination procedure, Tees and Symons (1987) trained rats to press one lever following a 2-second light signal and to press another lever following a 6-second light signal. When tested with sound signals of these two durations, it was found that the rats would respond according to the rule they had learnt during training with light. Moreover, transfer was also observed when the rats were trained with sound and tested with light. Hence, studies employing both the temporal generalization procedure and the choice discrimination procedure have demonstrated CMT of the amodal property of time in rats. Finally, CMT of space has also been demonstrated in normal rats. Tees and Buhrmann (1989) presented a light signal to either the right or the left visual field of the rats, and the rats had to respond according to one of two different spatial rules. For the ipsilateral rule, the rat had to press the lever to the same side as the light signal in order to receive a food reward; for the contralateral rule, the rat had to respond to the lever on the opposite side to the light signal. It was found that when tested with sound signals, the rats would respond using the rule they had acquired during initial training with light. However, unlike CMT of intensity or time, the rats did not perform very well on spatial CMT from sound to light. While the rats would demonstrate transfer from sound to light if they were initially trained using the ipsilateral rule, they did not show any transfer if the contralateral rule was used during the initial training using sound signals. Although the rats did not show perfect transfer in all conditions in the spatial CMT task employed by Tees and Buhrmann (1989), this task still appears to be an appropriate behavioural task that can be used to investigate the role of PPC in CMT for location in rats. This was the purpose of Experiment 3 of the present study. For the present study, the procedure used by Tees and Buhrmann (1989) was adopted. However, because transfer was poor from sound to light even for unlesioned rats, it was decided that only the transfer from light to sound would be tested. It was believed that this task would allow  25  the investigation of two different functions of PPC. The first function was related to the spatial role of PPC. PPC lesioned rats have been shown to be impaired on a variety of visuospatial tasks, so it would be interesting to find out if they would also have difficulties in acquiring the different spatial rules in response to the light signals in the initial training phase of the spatial CMT task. Secondly, during transfer from light to sound, performance of PPC lesioned rats would reveal whether PPC played any role in spatial CMT, in other words, whether PPC served any role in integrating spatial information from different sensory modalities. Purpose of the Present Study Evidence has accumulated in support of the involvement of PPC in visuospatial behaviours in a variety of behavioural tasks. In one behavioural task, the Morris water maze, PPC lesioned rats took longer to locate a hidden platform in a pool of water compared to control rats. However, spatial learning might still be possible in PPC lesioned rats because their performance appeared to improve over trials. Thus, in Experiment 1, the original water maze task was modified in order to examine the extent of the visuospatial deficits in PPC lesioned rats. Moreover, several behavioural measures were taken so that a more detailed analysis of the form of the deficits could be made. Because PPC receives inputs from sensory systems other than the visual system and spatial perception is believed to be a supramodal ability, the role of PPC in spatial behaviours involving other sensory modalities was postulated. In Experiment 2, the role of PPC in audiospatial behaviours was investigated using an open field which contained both visual and auditory objects. A previous study using the open field with only visual objects had revealed that PPC lesioned rats would not react to the relocation of the objects, whereas control rats would react to the change. Thus, in Experiment 2, this paradigm was extended to test whether PPC lesioned rats would react to the relocation if an auditory cue was attached to the displaced object. Even if PPC was found to play a role in spatial behaviours involving different sensory modalities, Experiment 2 would not allow a  26  clarification of whether spatial processes for different modalities were separate in PPC or they were integrated in PPC as a unitary percept. A more definite answer regarding these two different possibilities might be obtained by using a spatial CMT task, which tested whether the subjects could carry out intersensory associations so that spatial rules learnt in the initial visual training on the task could be utilized in the auditory transfer test. Thus, in Experiment 3, PPC lesioned rats were compared to control rats on this spatial CMT task. It was believed that this spatial CMT task could allow investigation of the roles of PPC in cross-modal matching for the amodal concept of space; moreover, performance of the rats in the initial visual training might also reveal visuospatial deficits commonly observed in PPC lesioned rats in other behavioural tasks.  EXPERIMENT 1: MORRIS WATER MAZE Method Subjects The subjects consisted of 20 male Long-Evans rats bred in colony facilities at the University of British Columbia. They had free access to food and water, and were maintained on a 12/12 hour light/dark cycle. When the subjects were around three to four months old, half of the subjects were randomly chosen to receive PPC lesion, and the other half received sham operation to serve as controls. Before the operations, all subjects were anesthetized using sodium pentobarbital (0.1 cc / 100 g, i.p). For the subjects chosen to receive PPC lesion, skull opening was made from 2 mm to 6 mm posterior to bregma, and from 1.5 mm to 5.5 mm lateral to the midline. These coordinates were adopted from Kolb and Walkey (1987), in which several anatomical techniques were used to identify that the cortical regions marked by these coordinates were the rat analog of the primate PPC. After skull opening was made, the exposed cortex was removed by aspiration, taking care not to damage the hippocampus. For the subjects chosen to receive sham operation, a midline incision was made in the  27  scalp, the skin and the underlying membrane were retracted, and then the incision was sutured together. After the operations, all subjects were allowed at least one month to recover before being subjected to behavioural testing. At the completion of behavioural testing, PPC lesioned rats were asphyxiated in a carbon dioxide chamber. Next, they were intracardially perfused with physiological saline, followed by formal saline. Their brains were removed and were stored in formal saline for at least 24 hours. The brains were then frozen and sliced at 40 um, with every fifth slice mounted on gelatine slides, and examined under a microscopic slide projector for verification of the lesion placement. Apparatus The water maze was a circular pool made of fibreglass and was painted white (180 cm in diameter, 60 cm in height). It was filled with water which was made opaque using white watercolour paint. A white cylindrical plastic container (13 cm in diameter, 18 cm in height), filled with stones and topped with a wire mesh, was used as the escape platform. The platform was placed inside the pool, and its top surface was below the surface of the water so that it was invisible to the subject in the pool. No attempt was made to prevent the subjects from using the distal visual cues available in the testing room. All the visual cues were kept constant throughout all testing days. The testing room was illuminated by three lamps mounted on two adjacent walls approximately 40 cm from the pool, and the lamps were mounted slightly below the top of the pool. An automated target tracking system was used to record each subject's performance on each trial. The subject was observed using a black-and-white video camera positioned above the centre of the pool, and the output of the camera was sent to an HVS image analysis unit (VPl 12) which calculated the X-Y coordinates of the position of the subject's head. The coordinates were sent to a 286 PC at the rate of 10 / sec and were recorded on a hard disk drive. Several measures of the subject's performance were obtained from the computer analysis of the data: escape latency, percentage of time spent  28  in each quadrant of the pool, and heading error. Moreover, the experimenter also recorded the strategy the subject utilized in searching for the hidden platform. The different strategies were: direct (the subject swam directly to the quadrant containing the platform once it was released into the pool), looping (the subject swam in a circular pattern in the pool and had crossed at least three quadrants before locating the platform), and random (all other swim patterns not described above, which usually consisted of the rat swimming in every part of the pool and making irregular changes in swim direction). Procedure Behavioural testing was conducted on seven consecutive days, with each rat receiving eight trials each day. During Trials 1 through 36 (Days 1 through 4, and the first four trials on Day 5), the platform was located in the centre of one of the quadrants of the pool; and during Trials 37 through 56 (the last four trials on Day 5, and Days 6 and 7), the platform was located in the centre of the diagonally opposite quadrant. Because the subjects were tested in batches of five rats on each trial, the platform location was different for adjacent subjects in order to eliminate the use of odor trails. This arrangement was used because despite earlier claims that odor cues were absent in the water maze (Sutherland & Dyck, 1984), a more recent study had shown that odor trails could be present in the water maze, and rats could learn to use such trails despite intact spatial abilities (Means, Alexander, & O'Neal, 1992). Thus, the platform location was different for adjacently tested rats in order to completely eliminate the possibility of the use of odor trails in locating the hidden platform. Each trial consisted of placing the subject by hand into the water facing the wall of the pool, at one of four starting locations: north, east, south, or west (see Figure 4). Within each block of four trials, each subject started at each of the starting locations, but the sequence of locations was chosen randomly. All subjects were tested using the same sequence of starting locations. If the subject found the platform on a trial, it was allowed to remain on the platform for 10 seconds. However, if the subject could not find the  29  Figure 4. The starting locations and the platform locations in the Morris water maze. The rats were released into the pool from four possible starting locations: N, E, S, and W (not true magnetic directions). Each rat was assigned a different platform location; the possible locations were at the centre of each quadrant of the pool as indicated by the circles.  30  platform, the trial was terminated after 90 seconds, and the subject was directed by the experimenter to the platform. At the end of a trial, the subject was removed from the pool, and was placed in a carrying cage for at least five minutes before the next trial began. Results Anatomical In general, the lesions were consistent across rats. The lesions were in the intended regions, and they were consistent in width and depth. For a sample of the lesion in an averaged rat, see Figure 5. Slight hippocampal damage was observed in only one of the rats. However, comparison of the behavioural data from this rat with other lesioned rats did not reveal a difference, and data from this rat were included in the statistical analyses. Behavioural Escape latency. The graph of escape latency (Figure 6) showed that although the PPC lesioned rats were slower than the control rats in locating the hidden platform on every trial block, both the lesioned and the control rats improved over trials. Moreover, the performance of the lesioned rats, like that of the control rats, was disrupted by the relocation of the platform. For each subject, the data for every four trials were averaged as a block, and a 2-way between-within ANOVA was conducted on the averaged data. The inferior performance of the PPC lesioned rats was confirmed by a significant treatment effect, F(l, 18) = 42.42, p < .001; and the improvement of the rats over trials was revealed by a significant block effect, F(13, 234) - 17.09, p < .001. The Treatment x Block interaction was not significant, F(13, 234) = 1.37, p > . 10, indicating that both PPC lesioned and control rats displayed similar patterns of performance improvement over trials and performance disruption following the relocation of the platform. Quadrant Stay. The percentage of time the rats spent in each quadrant of the pool seemed to tell a similar story as the escape latency (Figure 7). For the block before the  31  Figure 5. Representation of the posterior parietal cortex lesion in an averaged rat in the present study.  32  Figure 6. The escape latencies of PPC lesioned and control rats over the 14 trial blocks in the Morris water maze.  Treatment: *PPC O Control 70  60  Platform moved  \  A \  3 « oo $  .9 a  3  50 L \  7\  40  \  O  'o\  \\ \  30  wy  <D  B<  •—•  TO  [S3  20  ©..  o  o..  10  O.  G.  © O 0  J  1  2  J  L  3  4  5  °  '©•-  O-  12  13  o  L  6 7 8 9 10 Block of Four Trials  11  14  7. The percentage of time the rats spent in each quadrant of the Morris water maze. Preference for the quadrant initially containing the platform was found in both PPC lesioned and control rats on the blocks before (top) and after (bottom) platform relocation.  Before Relocation 80 70  60  Quadrants: I I Platform HBAdjacent (Anticlockwise) EDAdjacent (Clockwise) ^Opposite *  a p  J_  50  o  40 "S u  30 1111  20  !|!|lt!l!!  iii  10  • mm  0  PPC  Control  After Relocation 50  Quadrants; HI Platform (Previous) 023 Adjacent ESI Adjacent m Platform (Current)  40  a o  30  « SP "5 20 a* 10  PPC  Control  34  relocation of the platform, a 2-way between-within ANOVA performed on the percentage of time spent in the quadrants revealed a significant Treatment x Quadrant interaction, F(3, 54) = 16.20, p < .001. These percentages were then analysed using paired samples ttests. For the control rats, it was found that the percentage of time spent in the quadrant containing the hidden platform was significantly higher than that spent in the other quadrants, p's < .001. For the PPC lesioned rats, the percentage of time spent in the quadrant containing the platform was significantly higher than that in the opposite quadrant and one of the adjacent quadrants, p's < .01; and the difference between the stay in the quadrant containing the platform and the quadrant on its anticlockwise adjacent also approached significance, t(9) = 2.24, p = .052. Hence, the results seemed to indicate that all the rats had learnt the location of the platform before the platform was being relocated. For the percentages on the block after the relocation of the platform, a 2-way betweenwithin ANOVA was used to analyse these data. A significant quadrant effect was found, F(3, 54) = 13.76, p < .001; however, both the treatment effect and the Treatment x Quadrant interaction were not significant, F( 1, 18) = .55, p > .50, and F(3, 54) = 2.16, p > . 10, respectively. These results indicated that both the PPC lesioned and the control rats displayed a similar pattern of quadrant stay. Specifically, all the rats were spending most of the time in the quadrant which previously contained the hidden platform. The preference for the quadrant where the platform was previously located was confirmed by paired samples t-tests, p's < .02. Heading error. From the heading error (Figure 8), it could be seen that the control rats were becoming more accurate in heading towards the hidden platform over trials. Moreover, their heading error increased sharply after the relocation of the platform, indicating that they must be returning to the previous location to search for the hidden platform. On the other hand, the PPC lesioned rats had large heading error on every trial. The heading error of the lesioned rats did not seem to improve over the trials and was not affected much by the relocation of the platform. A 2-way between-within ANOVA  35  Figure 8. The heading errors of PPC lesioned and control rats over the 14 trial blocks in the Morris water maze.  Treatment: • PPC O Control  Platform moved 60  o m § 4 o / o. SP  /*,  Q \  50  0  II  0 0-0  S 30  "G-.  I—  w  Q  0  O 0  0  2 20  a: 10  o1  2  3  4  5  6 7 8 9 10 Block of Four Trials  11  12  13  14  36  Table 1. The number of PPC lesioned and control rats employing each search strategy on the trials before and after platform relocation in the Morris water maze.  Treatment  Search Strategy  PPC Lesioned  Control  Before Relocation  Direct  2  10  Looping  7  0  Random  1  0  After Relocation  Direct (Current)  1  1  Direct (Previous)  3  9  Looping  6  0  37  performed on the heading error confirmed the above observations: a significant Treatment x Block interaction was found, F(13, 234) = 2.56, p < .01. Search strategy. The search strategies employed by the rats in locating the hidden platform also seemed to reveal a navigational difficulty in the PPC lesioned rats as indicated by their heading error (Table 1). On the trial before the relocation of the platform, all the control rats were swimming directly to the location of the hidden platform once they were released into the pool. On the other hand, 7 of the 10 PPC lesioned rats were using a looping strategy. On the trial immediately after the relocation of the platform, 9 of the 10 control rats swam directly to the previous location of the hidden platform. However, only 3 PPC lesioned rats swam directly to the previous location. In fact, 6 of the 10 PPC lesioned rats were still using a looping strategy.  EXPERIMENT 2: OPEN FIELD Method Subjects The subjects consisted of 36 male Long-Evans rats bred in colony facilities at the University of British Columbia. They had free access to food and water, and were maintained on a 12/12 hour light/dark cycle. When the subjects were three to four months old, 20 of the subjects were randomly chosen to receive PPC lesion, and the remaining 16 subjects received sham operation to serve as controls. The surgical procedures were the same as that in Experiment 1. After the operations, all subjects were allowed at least one month to recover before being subjected to behavioural testing. Moreover, all subjects in this experiment also participated in Experiment 3. The order of participation in the two experiments was counterbalanced for subjects in both the lesioned and the control groups, and there was an interval of at least a month between participation in the two experiments. At the completion of behavioural testing, the PPC lesioned subjects were sacrificed using the same procedure as in Experiment 1 for verification of the lesion placement.  38  Apparatus The apparatus was a square open field, 120 x 120 cm with walls 30 cm high. It was made of wood and was painted white. Black lines (0.5 cm wide) were marked on the surface of the open field to divide it into 16 equal squares. These squares were used as references for the counting of the number of crossings made by the subjects in the open field. The open field was placed on a platform so that it was 68 cm above the floor. Curtains were used to completely surround the open field. The apparatus was illuminated by a lamp on the ceiling of the testing room. Three objects were placed in the open field. Object 1 was a multicolour cylindrical plastic container (11 cm in diameter, 13 cm in height). It contained a metronome (Seiko, SQM-300), which when switched on, produced an auditory cue with intensity of 57 dB and tempo of 50 beats per minute. Object 2 was a yellow and red egg-shaped plastic toy (largest diameter was 11 cm, height was 13 cm). Object 3 was a purple and beige cylindrical plastic container (8 cm in diameter, 20 cm in height). All objects were buried in clean bedding material when not used in order to control for olfactory differences. The same automated target tracking system used in Experiment 1 was used here. The only difference was that the coordinates of the rat's head were sent to the PC at the rate of 5 / sec. In order to allow for more precise tracking of the rat's head, the black fur on the rat's back was shaved approximately two days before open field testing occurred. A computer program was used to analyse the coordinates, and the time the subject was in contact with each object during each session was recorded. Moreover, the experimenter also counted the number of crossings (using a hand-tally counter) the subject made with reference to the 16 squares shown on the open field. The number of crossings was used as a measure of the locomotor activity of the subject in the open field. Procedure All subjects were tested on two phases: visual and auditory. The two phases were separated by one week, and the order of participation in the two phases was  39  counterbalanced for the subjects in both PPC lesioned and control groups. In each phase, each subject was individually tested on six consecutive six-minute sessions, with an interval of three minutes between sessions. The durations for the sessions and the intersession intervals were based on Save, Poucet, Foreman, and Buhot (1992), because significant habituation to the objects was observed in their rats. Moreover, another study had revealed that increasing exposure from one to three or five minutes had a positive effect on the response to a change in a T-maze, but further increases of exposure to ten and fifteen minutes did not result in larger response, and an increase of exposure to twenty minutes even reduced the response (Lukaszewska, 1978). Thus, it was believed in the present study that further increases in the session duration were not necessary for achieving better habituation. Figure 9 is an overview of the test sessions. During Session 1, the subject was allowed to explore freely in the empty open field, so that it could familiarize itself with the apparatus. During Sessions 2 through 4, the three objects were placed in the open field, and their locations remained constant during these three sessions. These three sessions allowed the subject to explore and habituate to the objects. During Sessions 5 and 6, the object containing the metronome (Object 1) was placed in a different location in order to test whether the subject would react to a spatial change. During all sessions of the visual phase, no auditory cue was used (i.e. the metronome inside Object 1 was switched off). However, during Sessions 2 through 6 of the auditory phase, the metronome was on. The open field was wiped with water before Session 1, and it was wiped without solvents before all other sessions. All the objects in the open field were touched by the experimenter before each session to control for olfactory cues. Each subject was always introduced into the open field at the same location facing the wall of the open field. Between sessions, the subject was removed from the open field and was left in a carrying cage where it could not see the open field. In the auditory phase, auditory cues from the metronome were turned off between sessions.  40  Figure 9. The testing procedure in the open field. The numbers within the circles represented the locations of the different objects. "Start" indicated the location the rat was released into the open field.  Session 1:  St£ rt  Sessions 2 - 4 :  <£rG> G> st; rt  Sessions 5 - 6 :  <L> &  <3> st rt  41  Results Anatomical In general, the lesions were consistent across subjects and were in the intended regions. The lesions were comparable to those in Experiment 1 (see Figure 5). One of the lesioned rats had extensive damages to the right hippocampus, and this rat had developed seizures. Thus, results from this rat were eliminated from all data analyses. Seven other PPC lesioned rats also had slight damage to the hippocampus, mostly on only one side of the hippocampus. In order to have a large number of subjects in each treatment group, data from these subjects were retained in the analyses. Behavioural Other than the PPC lesioned rat which had extensive right hippocampal damage, data from one control rat and four other PPC lesioned rats were also eliminated from the data analyses for the present experiment. The elimination of three of the four PPC lesioned rats was due to improper execution of the testing procedure. One lesioned and one control rat were eliminated because they demonstrated very little activity in the open field. Hence, the final data analyses for the present experiment consisted of 15 PPC lesioned and 15 control rats. Locomotor activity. In terms of locomotor activity, all rats seemed to have habituated over the six sessions in either the visual or the auditory phase (Figure 10). This observation was confirmed by the results of statistical analyses. In the visual phase, a 2way between-within ANOVA revealed a significant session effect, F(5, 140) = 16.74, p < .001, but the treatment effect and the Treatment x Session interaction were not significant, F(l, 28) = 1.08, p > .30, and F(5, 140) = 1.05, p > .30, respectively. In the auditory phase, a 2-way between-within ANOVA also showed the same pattern: the session effect was significant, F(5, 140) = 16.02, p < .001, but the treatment effect and the Treatment x Session interaction were not significant, F(l, 28) = 2.53, p > . 10, and F(5, 140) = .29, p > .90, respectively. The nonsignificant treatment and interaction effects  42  Figure 10. Locomotor activity of PPC lesioned and control rats over the six sessions in the open field. (Top: visual phase; bottom: auditory phase).  Visual Phase Objects introduced  Treatment: *PPC -Control Object moved  BO  .a o  a 55  Session  Auditory Phase  Treatment: • PPC -Control Object m o v e d  Objects introduced 70 60 * .9  50 -  W Cft  O  u  40 -  _————"* i - ^ ^  ^  ^  "  \  '"O-. .,  ^ \ ^ ^  30 -  s s  z  ~~~~-«  20 -  '•-'  10 0-  i  i  3  4 Session  i  43  indicated that there was no difference in the habituation of locomotor activity between PPC lesioned and control rats in either the visual or the auditory phase. Contact time for nondisplaced objects. The contact times for the nondisplaced objects (Objects 2 & 3) showed a similar pattern over sessions as locomotor activity. The contact times for these objects decreased gradually for all rats on both visual and auditory phases, and the rats did not show much reaction to these objects following the spatial change. Thus, only the contact time for the displaced object (Object 1) was subjected to further statistical analyses. Visual phase contact time. In the visual phase, both PPC lesioned and control rats demonstrated significant habituation to the displaced object over the three sessions before the spatial change (Figure 11). Indeed, a 2-way bet ween-within ANOVA conducted on the contact times on these three sessions revealed a significant session effect, F(2, 56) = 10.97, p < .001. However, the treatment effect, F(l, 28) = .001, p > .90, and Treatment x Session interaction, F(2, 56) = 2.45, p > .09, were not significant, indicating that the lesioned and the control rats displayed similar habituation. When this object was relocated on Session 5, the PPC lesioned rats and the control rats seemed to react differently. A 2way between-within ANOVA performed on the contact times for the displaced object on the session before and the session after the spatial change revealed a significant Treatment x Session interaction, F(l, 28) = 4.44, p < .05. A reaction score was then calculated for each rat by subtracting the contact time for the displaced object on the session after the spatial change by that before the change. An independent samples t-test performed on this reaction score showed a significant difference between the PPC lesioned and the control rats, t(28) = 2.11, p < .05 (Figure 12). Hence, these results seemed to show that while control rats reacted to the relocation of a visual object, PPC lesioned rats failed to do so. Auditory phase contact time. In the auditory phase, a 2-way between-within ANOVA performed on the contact time for the displaced object over the three sessions before the spatial change showed that the session effect was almost significant, F(2, 56) =  44  Figure 11. The contact time for the displaced object for PPC lesioned and control rats over the six sessions in the open field. (Top: visual phase; bottom: auditory phase).  Visual Phase Objects introduced  Treatment: *PPC •? Control Object moved  20 -i  "S o  .3,  1 3  Auditory Phase Objects introduced  20  a p  Object moved  15  10  1 6  Treatment: • PPC e Control  5 -  /  3  4 Session  45  Figure 12. The reactions of PPC lesioned and control rats towards the spatial change in the visual and the auditory phases. The reaction score was calculated by subtracting the contact time for the displaced object on the session after the spatial change by that before the spatial change.  *  VI  a o o 1/3  *-* o o a o T2 o  0  en  Treatment: ES3PPC •Control  <u  -2 -  -3 Visual Phase  Auditory Phase  46  2.74, p = .07. This result might indicate that habituation to the displaced object was less complete when an auditory cue was attached to this object. There was no significant treatment effect, F(l, 28) = 1.33, p > .20, and no significant Treatment x Session interaction, F(2, 56) = .47, p > .60. Thus, both the PPC lesioned and the control rats displayed a similar pattern of habituation (Figure 11). Following the spatial change, both PPC lesioned rats and control rats seemed to be reacting to the displaced object. Perhaps because of the incomplete habituation, a 2-way between-within ANOVA performed on the contact times for the displaced object on the sessions before and after the spatial change did not reveal any significant effect: treatment effect, F(l, 28) = .57, p > .40; session effect, F(l,28) = .36, p > .50; and Treatment x Session interaction, F(l, 28) = .03, p > .80. A reaction score was calculated for each rat as in the visual phase. Despite the failure of the ANOVA to reveal any significant reaction by the rats towards the spatial change, an independent samples t-test performed on the reaction scores showed that there was no significant difference between the lesioned and the control rats in their reaction towards the spatial change, t(28) = . 16, p > .80 (Figure 12).  EXPERIMENT 3: CROSS-MODAL TRANSFER Method Subjects The subjects were the same ones as in Experiment 2. There were 20 PPC lesioned rats and 16 control rats. The order of participation in the two experiments was counterbalanced for the subjects in both the PPC lesioned and the control groups, and there was an interval of at least one month between participation in the two experiments. Apparatus Three identical lever boxes (28 x 21 x 20 cm) were used. In each box, a food cup was placed in front of an opening in the front wall, where Noyes precision food pellets (45 mg) were delivered. Two retractable stainless steel levers (1.5 x 4 cm) were located 4 cm  47  above and 4 cm on the sides of the food cup, one on the right and the other on the left. A light emitting diode (LED) was located 4 cm above each lever, and a 4500 Hz sonalert was located 2 cm next to the LED on the side away from the food cup. Each lever box was housed in a large insulated chamber designed to minimize outside light and sound. In each chamber, a fan was used for ventilation. The three lever boxes were used simultaneously to test subjects, and were controlled by a 386 PC which used a DOS/ Windows multi-tasking environment. Computer programs written in C language monitored all activities and controlled the required levers, feeders, LED's, and sonalerts through a 96-line digital interface board. Moreover, at the end of testing for each rat on each day, the computer would display the number of correct and incorrect responses made by the rat to each lever. The experimenter would then make the following calculation: the number of correct responses was divided by the total number of responses to obtain a percentage correct score for each rat on each day. Procedure A few days before the start of shaping and testing, each subject was placed on a restricted feeding schedule. Once shaping and testing had started, the subject received just enough food in the home cage after shaping/testing, so that its weight was maintained at approximately 85 % of its normal weight. Shaping took five days. On the first day of shaping, each subject received one shaping session so that it could habituate to the apparatus. Each session began with the insertion of the left lever, ten presses to it were each reinforced by the delivery of a food pellet, and then the lever was retracted. Next, the right lever was inserted, ten responses to it were also reinforced, and the lever was retracted. After the retraction of the right lever, the left lever was inserted again, and the process continued until both levers were each inserted three times. If the subject did not press the levers, a food pellet was still delivered after each minute had elapsed, and the lever would retract after the delivery of ten pellets. On each of the remaining four shaping days, each subject received one to three  48  shaping sessions. During these sessions, the experimenter was present and would tap the levers once in a while in order to attract the subject's attention to press the levers. Once the subject had learnt to press the levers for food, the subject was left alone to finish the sessions. After the subject had completed the five days of shaping, testing began. During Days 1 through 21 of testing (initial training using light), light signals were presented through the LED's. Half of the rats in both PPC lesioned and control groups were trained to press the lever on the same side as the light signal in order to receive a food reward (i.e. respond to light using an ipsilateral rule), and the remaining subjects were trained to press the lever on the opposite side to the light signal (i.e. respond to light using a contralateral rule). During Days 22 through 28 of testing (CMT testing using sound), sound signals presented through the sonalerts were used instead of light signals. Moreover, half of the subjects in both ipsilateral and contralateral conditions were tested using the same rule as that during initial training (i.e. rule consistent condition), and the remaining subjects were tested using the other rule (i.e. rule inconsistent condition). Finally, on Day 29 of testing (final test using light and the original rule), each subject was tested again with the light signals. Moreover, the correct rule was the same one used in Days 1 through 21 during initial training (Figure 13). Each day of testing consisted of 100 trials. On each trial, the signal (light or sound) was on for two seconds, then both levers were inserted. If the subject pressed the correct lever, a food pellet was delivered. If the subject pressed the wrong lever, no pellet was delivered. If the subject did not press the levers, the levers were retracted automatically before the next trial began, and no food reward was given. The intertrial interval was chosen randomly from 20 to 90 seconds. Moreover, on each trial, the signal location was selected from the two available locations with equal probability, except for Days 1 through 5. During Days 1 through 5, a correction procedure was used so that if the response was incorrect on a trial, the same signal location was used for the next trial.  49  Figure 13. The experimental design of the spatial cross-modal transfer task.  PPC Lesioned Rats Control Rats  Days 1 to 21: (Initial Training Using Light)  Days 22 to 28: (CMT Testing Using Sound & New Rule)  Day 29: (Final Test Using Light & Original Rule)  Light Signals Ipsilateral Rule  Light Signals Contralateral Rule  Sound Signals Ipsilateral Rule  Sound Signals Contralateral Rule  Sound Signals Contralateral Rule  Sound Signals Ipsilateral Rule  Light Signals Ipsilateral Rule  Light Signals Ipsilateral Rule  Light Signals Contralateral Rule  Light Signals Contralateral Rule  Rule Consistent  Rule Inconsistent  Rule Consistent  Rule Inconsistent  50  Results Behavioural In addition to the PPC lesioned rat with extensive hippocampal damage, data from three other PPC lesioned rats were not used in the statistical analyses in the present experiment: one rat died on Day 28 of testing for no apparent reason; another rat's results for one of the testing days were missing; the third rat's data were not used so that there would be an equal number of subjects in each testing condition, and this rat was chosen randomly from the rats in the same testing condition. Thus, data from 16 PPC lesioned and 16 control rats were included in the statistical analyses in the present experiment, with 4 PPC lesioned and 4 control rats in each of the 4 testing conditions as shown in Figure 13. Initial training using light. A 3-way between-within ANOVA was performed on the percentage scores on Days 1 through 21, which consisted of the initial training using light signals (the between-subjects factors were treatment and rule, and the within-subjects factor was day). This revealed a significant treatment effect, F(l, 28) = 5.60, p < .03; rule effect, F(l, 28) = 6.22, p < .02; day effect, F(20, 560) = 153.27, p < .001; and Treatment x Day interaction, F(20, 560) = 1.80, p < .02. The significant rule effect was that the contralateral rule was more difficult to learn than the ipsilateral rule, and the significant day effect was that all rats were learning the task over the training days. From Figure 14, it seemed that the performance of the PPC lesioned rats was similar to that of the control rats in the initial and the final days of training using the light signals, however, the lesioned rats were learning slower and their performance lagged behind that of the control rats on the intermediate days. Results on Days 1, 5, 10, 15, and 20 were selected for closer examination and were subjected to independent samples t-tests. The outcomes of the ttests seemed to confirm the above observations: a significant difference between the lesioned and the control rats was found on Day 10, t(30) = 2.43, p < .03; but no significant difference was found on the other days, p's > .30. Finally, t-tests also  51  Figure 14. Performance of PPC lesioned and control rats on the spatial cross-modal transfer task. (Top: ipsilateral initial training; bottom: contralateral initial training).  CMT Testing Using Sound & New Rule  Initial Training Using Light & Ipsilateral Rule  100 -i  Final Test Using Light & Ipsilateral Rule  *-#-*"  80  a  rule consistent  o-o-  £ ^_  •  60  ©  chance  ^4  f ^ l H r ^ -----  40  20  • PPC (Rule Consistent) *PPC (Rule Inconsistent) -t> Control (Rule Consistent) -" Control (Rule Inconsistent)  Days 1-21  Days 22-28  Initial Training Using Light & Contralateral Rule  CMT Testing Using Sound &New Rule  Day 29  Final Test Using Light & Contralateral Rule  u O a u I*  u PH  Davs 1-21  Days 22-28  Day 29  52  confirmed that all rats were performing above chance level on the last day of training using the light signals, p's < .001. First CMT day using sound & new rule. On Day 22, when the signal was switched from light to sound and the new rules were applied, all the rats transferring to the ipsilateral rule were performing accurately, regardless of the rules they were initially trained to perform. On the other hand, the performance of all the rats transferring to the contralateral rule was greatly disrupted. A 3-way ANOVA was performed on the percentage scores on Day 22; and the three factors examined were treatment, response rule used before transfer, and response rule used after transfer. The ANOVA results confirmed the above observations, which revealed a significant effect of rule after transfer, F(l, 25) = 744.07, p < .001, but no other significant effects and interactions were found. Subsequent t-tests confirmed that all the rats transferring to the ipsilateral rule were performing significantly above chance, t(15) = 25.69, p < .001, but all those transferring to the contralateral rule were performing significantly below chance, t(15) = 14.30, p < .001. CMT training using sound & new rule. The performance of the rats transferring to the contralateral rule seemed to improve over days; however, they were still inferior to those transferring to the ipsilateral rule after seven days of training. This observation was confirmed by the statistical analyses. A 3-way ANOVA, similar to that used to analyse data on Day 22, was performed on the percentage scores on Day 28 (the last day of CMT training using the sound signals), and it was found that the significant effect of the rule used after transfer persisted, F(l, 25) = 60.07, p < .001, while all other effects and interactions remained nonsignificant. Despite the inferior performance of the rats using the contralateral rule, they were performing above chance on Day 28, t(15) = 4.59, p < .001, like those transferring to the ipsilateral rule, t(15) = 32.83, p < .001. Final test using light & original rule. When the light signal and the original rule were applied again on Day 29, all the rats appeared to have retained the original training. In fact, t-tests confirmed that all the rats were performing significantly above chance, p's <  53  .001. A 3-way ANOVA performed on the percentage scores on Day 29 (the three factors were treatment, rule during sound, and rule during light) revealed a significant treatment effect, F(l, 25) = 7.76, p = .01, as well as a significant effect of rule during light, F(l, 25) = 4.29, p < .05. Thus, it seemed that PPC lesioned rats were less capable than control rats in retaining the original training. Moreover, all the rats which were required to use the contralateral rule during CMT testing with the sound signals were not performing as well in the final test, compared to those using the ipsilateral rule with the sound signals.  DISCUSSION Morris Water Maze The results in the Morris water maze were consistent with that of other studies of the visuospatial function of PPC. In the Morris water maze, PPC lesioned rats were less capable than unoperated control rats in using the distal visual cues in the surroundings to locate a hidden escape platform. Specifically, PPC lesioned rats had a longer escape latency compared to control rats on every trial block. Indeed, many researchers have found that PPC lesioned rats have difficulties in utilizing the topographical relationships among places for navigational purposes; for example, deficits have been found in the Lashley III maze (Thomas & Weir, 1975), Hebb-Williams maze (Boyd & Thomas, 1977), radial arm maze (Kametani & Kesner, 1989; Kesner, DiMattia, & Crutcher, 1987; Kolb & Walkey, 1987), cheese board task (Kesner, Farnsworth, & DiMattia, 1989), open field (Save, Poucet, Foreman, & Buhot, 1992), as well as the Morris water maze (DiMattia & Kesner, 1988b; Kolb & Walkey, 1987). Despite the widely observed visuospatial deficits in the PPC lesioned rats, few investigators had attempted to examine closely the extent of this deficit. Specifically, a reduction in escape latency had been observed in PPC lesioned rats over trials in the Morris water maze. However, it was uncertain whether this improvement was due to learning the location of the platform or simply adopting a more efficient strategy to search  54  the pool. Studies employing the platform relocation test in the Morris water maze had not found unequivocal data to provide a definite conclusion. The present study extended the usual training phase of the place navigation task in the Morris water maze, and found that the performance of the PPC lesioned rats was disrupted as was that of the control rats by the relocation of the hidden platform. Moreover, a measure of the percentage of the time the rats spent in each quadrant of the pool revealed that both the PPC lesioned rats and the control rats were spending most of the time in the quadrant containing the platform before the relocation. After the relocation, all the rats would continue to search for the platform in this quadrant because they did not know that the platform had been relocated. Hence, if given enough opportunity to learn, PPC lesioned rats could acquire a spatial map of their surroundings, with their target properly located on this map. PPC lesioned rats seemed to have less severe visuospatial deficits than previous studies tended to indicate. However, PPC lesioned rats might still be deficient compared to control rats. It seemed that PPC lesioned rats were acquiring the spatial map more slowly than control rats. Moreover, the quality of this map might be poorer in the lesioned rats compared to the control rats. It is interesting to note that King and Corwin (1992) recently found a similar pattern of results using a cheeseboard task. The cheeseboard task was believed to be a land-based analog of the Morris water maze. In this task, a circular wooden board was used, and this board contained 177 uniformly spaced food wells. A food reward was placed in a food well located in the centre of one of the quadrants of the cheeseboard. Then, the rat was released onto the cheeseboard from one of the four possible start points around the perimeter of the cheeseboard, and the rat was allowed to search for the food reward. On the first 5 days, the food reward was always located in the same food well; and on the last 5 days, the reward was placed in a food well in the centre of the diagonally opposite quadrant. It was found that PPC lesioned rats traversed significantly longer distances than control rats in order to locate the food reward on most trials. Despite this impairment, PPC lesioned rats, like control rats, showed an improvement in performance  55  over trials. Moreover, when the food location was moved to the opposite quadrant, performance of both PPC lesioned and control rats was disrupted. All rats showed a sudden increase in path length. Although PPC lesioned rats were capable of learning the spatial location of a target, results from the cheeseboard task, as well as the present study using the Morris water maze, showed that the heading error of the PPC lesioned rats remained high over trials. This was in contrast to the control rats, which displayed a reduction of heading error over trials, with an appropriate significant increase only after the relocation of the target. Both studies also discovered that while control rats would go directly to the target location, PPC lesioned rats often displayed a looping pattern when moving towards the target. The large heading error of the PPC lesioned rats, which persisted over trials in both the Morris water maze and the cheeseboard task, was likely the result of the looping pattern of movement used by the lesioned rats. Moreover, the looping pattern might also account (at least partly) for the longer escape latency in the Morris water maze and the longer path length in the cheeseboard task for PPC lesioned rats over the testing trials. It was uncertain from the present study, as well as from previous studies, whether the looping pattern was a behavioural characteristic of the PPC lesion or was a behaviour adopted by the lesioned rats to compensate for other spatial deficits or navigational difficulties. The answer might lie in another hypothesis about a proposed role of PPC. According to this hypothesis, PPC is also involved in sensory-motor integration other than serving a spatial role. PPC receives sensory and motivational information from different cortical areas; and in return, it issues commands of a general nature for motor behaviours (Anderson, 1989; Stein, 1989). Such speculations are also supported by physiological findings. Some cells in the parietal lobe respond selectively to different combinations of movement and visual responses. For example, one type of cell appears to be active only if the rat makes a right turn at the same time as its lower nasal retina is stimulated by light (McNaughton, Leonard, & Chen, 1989). If PPC is really involved in sensory-motor  56  integration, damage to PPC will prevent the formation of the appropriate commands to direct behaviours, and abnormal movement patterns will result. Indeed, some researchers have shown that monkeys with damage to PPC have abnormal eye movement patterns, and they are impaired in directing their gaze voluntarily to targets (Brack & Gatesman, 1989; Ventre & Faugier-Grimaud, 1986). Moreover, studies of PPC lesioned human patients have also revealed impairments on visuomotor control tests. For example, PPC lesioned patients perform poorly if asked to use a pin to hit as quickly as possible some small circular target areas arranged in a row. When asked to reach for a glass bowl, the patients often displayed imprecise reaching behaviours (Pause, Kunesch, Binkofski, & Freund, 1989). It should be noted that the misreaching observed in the human patients seems to have some similarities with the looping behaviours of the rats in the Morris water maze and the cheeseboard task. This sensory-motor integration hypothesis has received further support. Recently, some researchers have even suggested that the primary role of PPC is in sensory-motor integration instead of spatial perception (Goodale & Milner, 1992). Indeed, some investigators have found that PPC lesioned subjects are capable of performing spatial tasks but are poor in sensory-motor coordination. For example, Pu, Ma, and Cai (1993) tested monkeys on a visual spatial delayed response task. The monkeys were first shown a food reward in one of two different locations, and after a delay, they were required to remember where the food was and to choose between the two locations. It was found that PPC lesioned monkeys were capable of performing this task. Despite a lack of deficit in short-term spatial memory, these monkeys were observed to misjudge distances and have difficulties in picking up food. Similar results have been found in the rats. McDaniel and Skeel (1993) found that PPC lesioned rats, like control rats, were able of using a cue located at the choice point of a water T maze to locate the alley containing an escape platform. However, PPC lesioned rats were impaired relative to control rats on an elevated rod walking/balancing task even after 12 days of training.  57  The results from the present study could also be used to support a role of PPC in sensory-motor integration because persistent heading error and the use of a looping search strategy was observed in the PPC lesioned rats. Although one might question a role of PPC in spatial behaviours because the lesioned rats could learn the location of the hidden platform as revealed by the disruption in escape latency and the percentage of time the rats spent in the original quadrant, the existing data are not persuasive enough to completely dismiss the spatial functions of PPC, when compared to the abundant data in support of the spatial role of PPC. In fact, it might be difficult to design tasks which could clearly dissociate spatial and navigational functions. Different tasks could also be testing different types of spatial behaviours. For example, the water T maze which the PPC lesioned rats were capable of (McDaniel & Skeel, 1993) might be a test of egocentric spatial behaviours, a kind of spatial behaviours which PPC has been shown not to play a role in (Kesner, Farnsworth, & DiMattia, 1989). In other words, the spatial tasks employed in some studies might not be sensitive enough to reveal the spatial deficits in PPC lesioned rats. Moreover, the spatial learning ability of PPC lesioned rats might also be mediated by other structures which normally play some roles in spatial behaviours, such as the different structures in the model of spatial representation (Kolb & Whishaw, 1990). Open Field Firstly, no significant difference in locomotor activity was found between the PPC lesioned rats and the control rats in either the visual phase or the auditory phase in the open field. This result is taken to indicate that although slight hippocampal damage was observed in some of the PPC lesioned rats in the present study, this hippocampal damage was not significant, because increased locomotor activity was commonly observed in hippocampal lesioned rats (Save, Poucet, Foreman, & Buhot, 1992). It is important to show that hippocampal damage was not significant in the study of the spatial functions of PPC because the hippocampus had also been suggested by many to play a role in spatial behaviours.  58  The results from the visual phase of the open field did confirm the findings of a previous study by Save, Poucet, Foreman, and Buhot (1992). In both studies, it was found that both PPC lesioned and control rats would habituate to a visuospatial arrangement of objects, and this habituation occurred in both locomotor activity and contact time for the objects. When one of the objects was moved, control rats would react to this change by an increase in contact time for the displaced objects. On the other hand, PPC lesioned rats appeared not to recognize the change, and their contact time for the displaced object continued to decrease over the sessions. These results seem to indicate that PPC plays a role in visuospatial behaviours, which are consistent with other work using different behavioural tasks to investigate the spatial functions of PPC. On the other hand, results from the auditory phase of the open field seem to contradict results of previous studies. Previously, researchers had found audiospatial deficits following PPC lesions in humans (Farah et al., 1989; Pinek et al., 1989) as well as in rats (Crowne et al., 1986). However, the results of the present study seem to indicate that such deficits are not evident on all tasks. Although the analyses showed that the increase in the contact time was not significant for both the control and the PPC lesioned rats following the relocation of the object containing an auditory cue, this increase, when compared to the gradual reduction in contact time in the other sessions, seems to indicate that both the control and the PPC lesioned rats did notice the relocation. Moreover, analyses of a reaction score, which was calculated by taking the difference in contact time for the displaced object between the sessions before and after the relocation, indicated that there was no difference between the reaction in control rats and PPC lesioned rats. Because PPC lesioned rats would not react to the same pattern of spatial rearrangement using the same objects in the visual phase, the reaction observed in the auditory phase must be the result of the additional auditory cue attached to the displaced object. The ability of the PPC lesioned rats to react selectively to this auditory cue indicates that  59  auditory localization was possible in these rats, and this result seems to suggest that PPC is not involved in certain kinds of audiospatial behaviours. The conclusion that PPC does not play a role in audiospatial behaviours should be considered tentative. It should be pointed out that although the same objects and testing procedure were used in both the visual and the auditory phase in the open field, the auditory phase was not an exact analog of the visual phase. While all the objects in the visual phase served as different visual stimuli occupying different spatial locations, they were equal in the auditory modality since they were not consistently associated with any auditory cue. Through exploration, the rats could acquire a representation of the visuospatial relationship among these objects. Reactions by the rats following object relocation were likely the results of recognition of a change in this visuospatial representation. A comparable auditory phase should consist of the same number of objects as in the visual phase, serving as different auditory stimuli while being equal in the visual modality. For example, three objects producing different auditory signals should be used. The visual and the tactile characteristics of these objects could be equated by hiding these objects in similar containers. Moreover, because auditory stimulation was absent in the visual phase, visual stimulation could be eliminated from the auditory phase by testing the rats in darkness. However, in the auditory phase of the present study, only one of the objects served as a single auditory stimulus, and these objects were serving as different visual stimuli. It was unlikely that an audiospatial representation, like the visuospatial representation in the visual phase, could be acquired by the rats using only a single auditory stimulus. The spatial abilities required in the auditory phase should be less complex than that in the visual phase. While localization of a lone sound source was sufficient in the auditory phase; in the visual phase, the rats had to recognize that there were several different visual stimuli each occupying a different location, remember the spatial relationship among these stimuli, notice that the relationship was changed, compare the new location of each object with its previous location in memory, in order to react  60  selectively to the relocated object. It is possible that if the spatial demand of the auditory phase was raised to a level comparable to that of the visual phase, an audiospatial deficit might also be found in the PPC lesioned rats. The performance of the PPC lesioned rats in the auditory phase of the present experiment could also simply be the result of increased object saliency. Improved performance by brain lesioned rats following increased stimulus saliency has been demonstrated by previous studies. In a study by Davis and McDaniel (1993), a cue was located at the choice point of a water T maze to signal which of the two alleys contained the escape platform. A grey card was used as the cue to signal one of the alleys, and a white card was used to signal the other alley. While control rats could learn to perform this task, PPC lesioned rats were significantly impaired. However, completely different results were found after slight modifications were made to the task in another study by the same group of researchers (McDaniel & Skeel, 1993). Specifically, a black card was used instead of the gray card in order to increase cue saliency. Moreover, the rats were punished by confinement to the incorrect arm instead of being allowed to self-correct for incorrect choices as in the previous study. After such modifications were made, the PPC lesioned rats were found to have equal performance as the control rats. Midgley and Tees (1981) also found a similar effect when investigating the functions of the superior colliculus, a subcortical brain structure which is believed to play a role in orienting behaviours. In their study, a ranking of the saliency of three different patterns of light displays was done based on the orienting behaviours of the control rats. It was found that rats with lesions of the superior colliculi would not respond to the less salient displays, whereas control rats would. However, both lesioned and control rats would respond to the more salient displays. Furthermore, when the presentation of the displays was paired with footshock in a subsequent experiment (Midgley, Wilkie, & Tees, 1988), the lesioned rats would also respond to the less salient displays. Hence, stimulus saliency and motivational factors are both important variables which can affect the performance of  61  brain lesioned rats. Interestingly, in the original experiment by Midgley and Tees (1981), auditory displays which were analogs of the less salient visual displays were also presented to the rats. It was found that the superior colliculi lesioned rats, which would normally not respond to these visual analogs, would respond readily like the control rats to the auditory displays. Thus, auditory stimuli, which were supposed to be analogs of certain visual stimuli, might actually be more salient to the rats than their visual analogs. In the open field, increasing stimulus saliency by attaching an auditory cue to the displaced object might induce reactions from the PPC lesioned rats. Before a consideration of the issue of stimulus saliency, reactions by the lesioned rats on the auditory test could be taken as evidence to indicate that PPC was not essential to the display of audiospatial behaviours, whereas the lack of reactions on the visual test indicated that PPC was necessary for visuospatial behaviours. However, the demonstration that reactions could be induced by increasing stimulus saliency might imply that PPC lesioned rats could actually detect the spatial change in both the visual and the auditory phases, but the lesioned rats would only react when the objects were more salient as in the auditory phase. Thus, the deficit in the PPC lesioned rats might be an attentional one instead of a detection one, and PPC might be involved in spatial attention instead of spatial location. Obviously, future studies should be done with carefully designed procedures for both the visual and the auditory tests, in order to clarify the role of PPC in audiospatial as well as visuospatial behaviours. One final point worth mentioning regards the incomplete habituation in contact time before the object relocation in the auditory phase of the present open field experiment. Although the contact time for the displaced object appeared to decrease over the three sessions before the spatial change, statistical analyses showed that this reduction did not reach significance (p = .07). Like the reaction observed in the auditory phase, this nonsignificant habituation might also be the result of the increased stimulus saliency caused by the addition of the auditory cue. In fact, some researchers seem to have found a  62  similar effect using a different open field paradigm to test PPC lesioned and control rats. Control rats were found to react by renewed exploration of a missing object in the open field, whereas PPC lesioned rats did not respond to this change. However, when another object was placed next to the location of the "missing" object, PPC lesioned rats would spend a high amount of time exploring that location in all sessions even though no further increase in exploration was observed following the removal of the "missing" object. Hence, associating an additional object to the "missing" object might be responsible for maintaining a high level of interest and responsiveness in PPC lesioned rats (Save, Buhot, Foreman, & Thinus-Blanc, 1992). In a similar vein, the addition of an auditory cue in the auditory phase of the present experiment might be responsible for the maintenance of a high contact time by the rats over the sessions. Intuitively, it seemed that the best way to deal with incomplete habituation was to increase the duration or the number of the sessions. However, pilot work was done prior to the present study, using different combinations of session duration and number, in order to achieve better habituation. Interestingly, it was found that the best way to achieve "habituation" was to use a larger sample size. Normally, individual rats display large variations in behaviours in the open field. For example, some rats demonstrate very little activity in the open field, individual rats have preference for different objects, and some rats may have noticed the change but were fearful to react. Using a larger sample size could reduce the impact of these individual differences. The present study consisted of 15 lesioned and 15 control rats in both the visual and the auditory phases, and future studies should certainly employ a larger number of subjects in order to obtain significant results in the open field. Cross-Modal Transfer The results from the initial training days of the CMT task seemed to reveal a pattern similar to that in other studies of the visuospatial functions of PPC. In the present study, both PPC lesioned rats and control rats were performing randomly on the first few days of training using the light signals. However, later on, the performance of the PPC  63  lesioned rats fell behind that of the control rats. The PPC lesioned rats were slower than the control rats in learning to use the different spatial rules in response to the light signals. This inferior performance of the PPC lesioned rats seemed to indicate a role of PPC in visuospatial behaviours. Despite this impairment, PPC lesioned rats eventually achieved the same level of performance as control rats, such that all rats had learnt the task and were performing comparably before being subjected to the transfer tests. In a way, the progress made by the PPC lesioned rats in this CMT experiment seemed to be consistent with that observed in the Morris water maze. The PPC lesioned rats appeared to be impaired relative to the control rats initially. However, if given enough training, PPC lesioned rats could also learn the spatial task as control rats did. Once again, it could be concluded that PPC might play a lesser role in visuospatial behaviours as most studies tend to indicate. However, the spatial abilities displayed by the PPC lesioned rats might also be the result of employing alternative unaffected strategies or brain structures to compensate for the spatial deficits caused by PPC lesions. The impairment in the PPC lesioned rats observed during the initial training seemed to be especially obvious during the acquisition of the contralateral rule than that of the ipsilateral rule. This finding seems to be consistent with results from previous studies using the Morris water maze. Previously, it had been found that PPC lesioned rats were as capable as control rats in locating an escape platform in the Morris water maze if the platform was visible. However, PPC lesioned rats were impaired relative to control rats if the platform was invisible and the platform location was only indicated by a visual cue located on the wall of the pool behind the platform. Hence, spatial deficits were observed in the PPC lesioned rats only when the cue signaling the target location was situated far away from the target (Kolb & Walkey, 1987). Indeed, the present study showed that while the impairment in performance of PPC lesioned rats relative to control rats appeared to be mild when the rats had to respond to the lever on the same side as the light signal,  64  this impairment was more obvious when the rats had to respond to the lever on the opposite side to the light signal. For the control rats which had learnt to respond to the light signals using the ipsilateral rule, a maintenance of performance was observed if the ipsilateral rule was used on the first day of the transfer test using the sound signals. This maintenance of performance was evidence of significant positive transfer in the rule consistent condition. On the other hand, if the contralateral rule was used with the sound signals, a disruption of performance was observed. In fact, the performance of these rats was below chance level. This below-chance performance indicated that the rats were still employing the ipsilateral rule to respond to the sound signals, and it was evidence of significant negative transfer in the rule inconsistent condition. The significant positive transfer in the rule consistent condition coupled with the significant negative transfer in the rule inconsistent condition are believed to reflect true CMT abilities in the rats (Tees & Buhrmann, 1989). Despite the positive and negative transfer observed in the control rats with the ipsilateral initial training, rats which had obtained contralateral initial training did not demonstrate true positive and negative transfer to the sound signals in the present study. Instead, these rats with the contralateral initial training had an above-chance performance if they were required to use the ipsilateral rule with the sound signals (no negative transfer in rule inconsistent condition), and they had a below-chance performance if they had to use the previous contralateral rule with the sound signals (no positive transfer in the rule consistent condition). Despite the failure to demonstrate true transfer in this instance, these rats were not performing at chance level after the transfer to sound took place. So, the performance of the rats was affected by knowledge they had gained during the light training on the sound transfer tests; however, the rats did not follow the original rules strictly. Instead, they could respond using different rules when the signals were from different sensory modalities. Such a result is different from that of previous studies, and it may indicate some weaknesses of the present spatial CMT task. In any case, performance  65  of the PPC lesioned rats on the transfer tests was similar to that of the control rats. On the tests which control rats had demonstrated positive and negative transfer, PPC lesioned rats were equally capable in demonstrating transfer, and thus it seemed that PPC might not play a role in spatial CMT. This conclusion seems to be consistent with that of the open field results, which revealed that PPC was not involved in audiospatial behaviours. Hence, although PPC receives inputs from different sensory modalities, it might not play a role in spatial behaviours involving sensory modalities other than vision, and thus it is not the site for a supramodal spatial mechanism. The CMT results further indicate that PPC was also not responsible for associating spatial information gained through different sensory modalities. The conclusion that PPC is not necessary for CMT should be considered tentative since the present spatial CMT task might not be a true test of CMT. Specifically, rats which had received contralateral initial training failed to demonstrate significant positive and negative transfer. In fact, there has been early criticism of some reports of successful demonstrations of CMT in rats. For example, the positive and negative transfer found in some studies was actually inferred by comparing the performance of the rats in the rule consistent condition with that of the rule inconsistent condition on the transfer tests, instead of comparing each condition with chance level. Moreover, the apparent transfer in some CMT tasks might be mediated by responses to different compound stimuli formed by combining the signal stimuli with the background stimuli (Tees, in press). Although the involvement of alternative mediators in the transfer observed in the present spatial CMT task is not certain, it is possible that a different spatial CMT task might reveal an impairment in the PPC lesioned rats. It should be interesting to note that a previous study employing the same spatial CMT task as the present study had found positive and negative transfer in the unlesioned rats which had received contralateral training (Tees & Buhrmann, 1989). These contradictions should be clarified in future studies.  66  On the final test day when the light signals and the original spatial rules were again used, all rats were performing above chance level. Although all the rats were also performing above chance level on the day before the final test, their performance was not disrupted on the final test day if a change in the spatial rule was involved. Specifically, the rats which had learnt to used the contralateral rule with the sound signals would use the ipsilateral rule with the light signals on the final test day, provided that they were trained to use the ipsilateral rule during the initial training with the light signals. Moreover, those rats which had learnt to use the ipsilateral rule with the sound signals would use the contralateral rule with the light signals on the final test day, given that they had received contralateral initial training with the light signals. The above seems to show that the rats in the present study had retained the original training despite seven days of training using different signals and rules. Moreover, they could simultaneously use different spatial rules for test signals coming from different sensory modalities. The retention of the original training and the simultaneous use of different spatial rules were also found by Tees and Buhrmann (1989). However, such results were not found in the case of CMT of duration, in which successful transfer was demonstrated by normal rats (Tees & Symons, 1987). These observations might further indicate that the recognition of the amodal property of location by normal rats is less evident than CMT of the amodal property of duration. Despite the weaknesses in the spatial CMT task employed in the present study, PPC lesioned rats were found to be impaired relative to the control rats on the final test day. Because no impairment was observed after the first (CMT) transfer, but was observed after the second transfer to signals of original training modality, it seems that PPC lesioned rats are less capable than control rats in simultaneously retaining different spatial response rules for signals coming from different sensory modalities. Hence, PPC might be involved in resolving intermodal conflicts of spatial information, instead of playing a role in CMT. In fact, some investigators have found such a higher order function of PPC in another domain. Previously, it was believed that unilateral PPC lesion  67  would cause neglect to the contralateral space. However, in a later study, rats with unilateral PPC lesions were found to be equally capable of turning towards signals presented on either side of their body. It was only when the signals were presented to both sides simultaneously that the rats displayed a preferential turning response to the ipsilateral side, and neglected the contralateral side. The authors concluded that lower systems were responsible for the immediate orientation to the signals, whereas PPC served a higher order function which was to resolve interhemispheric competition and to decide where attention should be directed (Save, Thinus-Blanc, & Buhot, 1992). In a similar vein, responses to the light and the sound signals in the spatial CMT task might be mediated by lower brain structures, and PPC might play a role in resolving the conflicts in the rules used for signals coming from different sensory modalities. Summary Results from the present study confirmed those of previous studies in revealing a role of PPC in visuospatial behaviours. Specifically, visuospatial deficits were found in PPC Iesioned rats in the Morris water maze, the open field, as well as the spatial CMT task. However, results from the Morris water maze and the spatial CMT task also showed that this visuospatial deficit might be less severe than previous studies suggest. When allowed sufficient training, PPC Iesioned rats could learn to use the topographic relationship among visual cues in the surroundings to locate a hidden platform in the Morris water maze, and these rats could learn to respond to light signals using different spatial rules in the CMT task. This mild visuospatial deficit was in contrast to a persistent navigational difficulty observed in the PPC Iesioned rats in the Morris water maze. Although PPC Iesioned rats could learn the location of a target, their navigation towards the target was poor, and they had to reach the target by following a looping pattern of movements around the target. Thus, it seemed that PPC also played a role in sensorymotor integration as suggested by some researchers. Because PPC received sensory inputs from different modalities, it was postulated that PPC was involved in spatial  68  behaviours in sensory modalities other than vision. However, results from the open field of the present study seemed to indicate that PPC did not play a role in audiospatial behaviours. Such results also did not support the hypothesis that PPC was the site of a supramodal spatial mechanism. Moreover, results from the CMT experiment further indicated that PPC was not responsible for associating spatial knowledge gained through visual modality with that of the auditory modality. Hence, PPC was not necessary in spatial CMT. 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