IMPACT OF SCOPOLAMINE AND YOHIMBINE ON PAIN REACTIVITY AND SHOCK-INDUCED ANTINOCICEPTION IN SPINALIZED RATS. P.S. Chen*, P.A. Illich, M.W. Meagher, & J.W. Grau. Dept. of Psychology, Texas A&M Univ., College Station, TX 77843.

We have previously shown that exposure to three brief (2 sec) 3.0 mA tail-shocks elicits an opioid antinociception, and that longer (75 sec) tail-shocks elicit a nonopioid antinociception in spinalized rats. The present experiments evaluate whether cholinergic or noradrenergic systems play a role in the production of these antinociceptive effects. In both experiments, subjects were spinalized at T2 and tested 8-10 hr later. Fifteen min after subjects received the test drug, or its vehicle, 3 tail-flick tests were performed to establish baseline levels of nociception. Subjects then received either no shock, 3 brief (2-s), or 3 long (75-s) 3.0 mA tail-shocks, after which nociception was assessed 5 more times with the tail-flick test. We found that the cholinergic antagonist scopolamine (1 mg/kg) decreased baseline tail-flick latencies. A similar effect has been observed in intact subjects (e.g. Grau et al., Behav. Neurosci., 105, 62, 1991). Scopolamine did not, however, affect the magnitude of either brief or long-shock induced antinociception. In contrast, the alpha-2-noradrenergic antagonist yohimbine (10 mg/kg) attenuated the antinociception observed after both shock schedules without affecting baseline tail-flick latencies. We are currently assessing the impact of intrathecal application of these drugs and the role of other neurochemical systems.

Published in Society for Neuroscience Abstracts, 17, 1991.

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