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Antinociceptive and other behavioural effects of abnormal vestibular stimulation in the rat Gray, David Shaun


Exposure to abnormal motion produces a variety of behavioural effects in both human and non-human species. The general purpose of the present studies was to produce and investigate some of these effects in the laboratory rat. In the first series of experiments, rats displayed appreciable decreases in reactivity to noxious stimuli presented after exposure to brief periods of different types of motion. This motion-induced antinociception was found to persist for periods of up to 15 min. A second series of experiments examined the role of the vestibular system in this motion-induced antinociception phenomenon. Rats whose peripheral vestibular apparatus had been rendered insensitive to accelerative stimuli did not exhibit motion-induced antinociception. Subsequent experiments attempted to delineate the role of some individual components of the central vestibular system but no single component investigated was found to play a major role in the production of antinociception. Experiments in this and the preceding series of experiments also demonstrated that the antinociceptive effect could be dissociated from dizziness or acute vestibular dysfunction. In the third series of experiments, the physiological mechanisms by which vestibular stimulation produces antinociception were investigated. Experiments in this series demonstrated that motion-induced antinociception could be blocked by opiate antagonists and that the motion-induced antinociceptive effect showed cross-tolerance with chronic morphine administration. These two findings strongly implicate an endogenous opiate peptide (endorphin) system as the underlying mechanism for mot ion-induced antinociception. The brief duration of the antinociceptive effect and the fact that disruption of the pituitary-adrenal axis did not affect motion-induced antinociception suggested that the opiate peptides involved were the enkephalins rather than B-endorphin. Other behavioural effects of abnormal motion were reported in the the fourth series of experiments. The resemblance between the symptoms of motion sickness and those of opiate administration suggested that endogenous opiate peptides may mediate motion sickness. Although exposure to abnormal motion did produce a substantial conditioned taste aversion (a behavioural assay for motion sickness in the rat), attempts to attenuate the aversion with two different opiate antagonists were unsuccessful. These results suggested that abnormal motion exerts its illness-producing effects through some mechanism other than an endogenous opiate system. In the final experiment, rats that were exposed to a brief period of abnormal motion subsequently exhibited a suppression of defensive burying behaviour that was similar to that produced by anxiolytic drugs. The results of this study indicate that abnormal vestibular stimulation may have a variety of different behavioural effects in rats. However, it appears that no single mechanism can account for all of these effects.

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