MILD SHOCK PRODUCES AN UNCONDITIONED, NALTREXONE-INSENSITIVE INCREASE IN REACTIVITY ON THE VOCALIZATION MAGNITUDE AND THRESHOLD TESTS. P.A. Illich*, C. W. Parker III., K.D. Burks, & J.W. Grau. Dept. of Psychology, Texas A&M Univ. College Station, TX 77843.

Prior work suggests that an aversive event can produce either an increase (hyperalgesia) or decrease(hypoalgesia) in pain reactivity. Although stress-induced hypoalgesia has been extensively examined both at the behavioral and neural levels, relatively little is known about stress-induced hyperalgesia. Here, we first establish a paradigm that produces a robust increase in responding to pain. Subjects experienced either mild shock (3, 0.75-s, 1.0mA) or nothing, and were then given a single test shock (0.75-s, 1.0mA). Previously shocked subjects vocalized more to the test shock relative to unshocked controls. A second set of subjects were treated the same except that vocalization threshold rather than magnitude was assessed. Shocked subjects exhibited a substantial decrease in vocalization threshold (hyperreactivity) that decayed over time (Experiment 2), irrespective of whether they remained in the shock-context (Experiment 3). Experiment 4 showed that this effect was naltrexone (14 mg/kg) insensitive. The results suggest that mild shock can produce an unconditioned, naltrexone-independent, increase in responding on the shock-induced vocalization and vocalization threshold tests. We are currently exploring the neural mechanisms that underlie this effect. Supported by BRSG 2S07RR07090 to J.W.G.

Published in Society for Neuroscience Abstracts, 18, 1992, 1026.

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