The role of the cerebellum in motor function is well documented. Additional data clearly im· plicate the cerebellum in the regulation of sensory processes and autonomic functions, and more recent findings establish an influence of cerebellar systems on the regulation of emotional and motivational behaviors. The cerebellum provides extensive projections to brain· stem and limbic mechanisms that have been implicated in behavioral regulation, and experimen· tal manipulations of the cerebellum have been found to profoundly affect behavioral processes. In the present paper, w~ review some of these findings and offer a conceptual view of cerebellar function that reconciles these apparently disparate actions. We suggest that the cerebellum exerts functionally similar influences at all levels of sensorimotor and behavioral orga· nization. This model provides a conceptual framework for understanding the behavioral consequences of cerebellar dysfunctions, which we suggest can be viewed as behavioral parallels to the classical cerebellar motor syndromes. Data implicating cerebellar systems in the pathogenesis of developmental disturbances in behavioral processes are also considered in the con· text of the present conception of cerebellar·behavioral function.
Systemically administered lysine-8-vasopressin (LVP; 16-128 micrograms/kg) was found to induce a potent and dose-dependent antinociceptive effect, as measured by the tail-flick test in the rat. This effect could be seen in the absence of any significant change in general activity, indicating that it was not due to sedation or general motor debilitation. The antinociceptive effect of LVP does not appear to be mediated by endogenous opiates or other pituitary hormones, as evidenced by: 1) the lack of antagonism by the opiate receptor blocker naloxone, 2) the lack of cross-tolerance with morphine, and 3) its persistence after hypophysectomy. Des-glycinamide-LVP, a vasopressin analog with no appreciable pressor or antidiuretic action, showed no antinociceptive activity (128 micrograms/kg), and des-amino-arginine-vasopressin, a vasopressin analog with minimal pressor activity but greatly enhanced antidiuretic activity, was also relatively ineffective (128 micrograms/kg). These results suggest that the antinociceptive activity of vasopressin may be related to receptor types similar to those mediating its pressor effects. Nevertheless, the antinociceptive action of vasopressin does not appear to be secondary to its pressor activity, since phenylephrine failed to induce an antinociceptive effect at a dosage that mimicked the pressor response to vasopressin. These results are in concert with a growing body of evidence suggesting that vasopressin may be one of several nonopiate peptides that play a role in the modulation of pain sensitivity.
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