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Effects of localized brain stimulation on conditioned taste aversion in rats

University of British Columbia

Conditioned taste aversions occur in rats if ingestion of a novel flavored solution is followed by toxicosis. Previous studies, employing the technique of localized brain stimulation to examine the neural correlates of this behavior, have shown that stimulation applied to restricted areas of the limbic system disrupts the subsequent aversion. The present series of experiments confirmed and extended the results of earlier reports, but challenged the interpretation of those results. Whereas the deficits in taste aversions were attributed previously to the disruption of memory functions, the present experiments showed that such learning could in fact occur in the presence of localized electrical stimulation of the brain (ESB). It was concluded that ESB may have cue properties similar to those of a novel flavor, resulting in a conditioned aversion to "stimulation-flavored" water. Some of the apparent deficits in taste aversion learning could be reinterpreted as results of stimulus control by the brain stimulation cue. Experiment I sought to confirm earlier reports of the effects of ESB of the amygdala (a complex of nuclei in the limbic system) on conditioned taste aversion (CTA) and to extend these findings to two nuclei of the extrapyramidal system, the caudate and substantia nigra, primarily associated with motor functions. These effects were compared with the effects of ESB on a passive avoidance response, in order to observe the result of similar treatments on another task requiring the animals to withhold responding. ESB applied to any of the three sites during acquisition of the passive avoidance behavior produced deficits in the response when tested 24 hr later. ESB applied during taste aversion conditioning, however, produced deficits in the subsequent CTA, tested 48 hr later, only when the amygdala was stimulated. These results suggested that the effects of localized extrapyramidal stimulation on passive avoidance behavior do not generalize to taste aversion. Experiment II sought to examine in greater detail the nature of the effects of amygdaloid stimulation on CTA. Stimulation applied while rats were drinking a novel solution (saccharin), during the time interval after the withdrawal of the solution, or immediately after the injection of the toxin, (lithium chloride) produced deficits in the subsequent CTA. Stimulation applied during the saccharin drinking in the 48-hr retest, or during saccharin drinking both in the conditioning and in the retest sessions, did not reduce the aversion to saccharin. The latter results suggested that taste aversion learning could occur in the presence of concurrent ESB and implied that memory processes also may have been intact in Experiment I. Experiment III sought to examine the possibility that amygdaloid stimulation may act as a cue or conditioned stimulus in a taste aversion paradigm. Rats were stimulated while drinking unflavored water and injected with lithium 10 min later. When retested after 48 hr, with stimulation applied during water presentation, water intake was suppressed by 60%. Water intake, retested with concurrent ESB at subsequent 48 hr intervals, recovered to the pre-lithium level by the eighth day after conditioning. This recovery appeared to be a function of the extinction of a conditioned aversion, similar to that seen in a group of animals with an aversion conditioned to saccharin. Water intake in the intervening days was unaffected, suggesting that an aversion had been conditioned to "stimulation-flavored" water and not simply to unflavored water. Unpoisoned and unstimulated controls showed no systematic suppression nor did caudate controls. These results suggest that amygdaloid stimulation provided a cue for lithium illness, and in Experiment II an aversion was conditioned to a stimulus compound consisting of taste and stimulation elements.

Text

2010-02-26

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http://hdl.handle.net/2429/21104

Psychology

University of British Columbia

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