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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Lesions of the fastigial nuclei and cerebellar vermis, but not lesions of the dentate nuclei, were found to produce marked performance deficits on a differential reinforcement of low rates (DRL) schedule of reinforcement. This deficit was characterized by an abnormal number and distribution of responses within the schedule interval. Lesions, however, did not produce a deficit following preoperative training or when subjects were tested on a fixed-interval (FI) schedule. In addition, when DRL and FI performance was contrasted, all subjects were responsive to schedule contingencies. Results suggest that the DRL deficit following cerebellar lesions is due to a tendency to perseverate in response strategies, and is not related to a global disruption of timing or a pervasive inability to suppress responding.

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