AMYGDALA LESIONS BLOCK SHOCK-INDUCED HYPERALGESIA IN RATS. E.D. Crown*, T.E. King, M.W. Meagher, J.W. Grau. Dept. of Psychology, Texas A&M University, College Station, TX 77843.
Exposure to a few moderately intense tailshocks has opposite effects on two measures of pain reactivity in rats (King et. al, 1996). Vocalization thresholds to radiant heat and to shock are lowered (hyperalgesia), while tail-withdrawal from radiant heat is inhibited (antinociception).
The current experiments examine the role of the amygdala in shock-induced hyperalgesia and antinociception. Experiment 1 tested the impact of excitotoxic lesions to the central amygdaloid nuclei on reactivity to radiant heat. Two weeks after surgery, rats were placed in restraining tubes and half of the rats in each condition received three 1-mA (.75s) tailshocks or an equivalent period of restraint. Tail flick and vocalization latencies to radiant heat were then measured two and eight minutes after the tailshocks. Bilateral lesions reduced vocalizations to radiant heat and blocked the induction of both shock-induced hyperalgesia and antinociception. Experiment 2 assessed the impact of central nuclei lesions on hyperalgesia as measured by vocalization to shock. Lesions to the central nuclei attenuated the hyperalgesia normally observed two minutes after shock. We are also examining the impact of lesioning the bed nucleus of the stria terminalis (BNST) and the basolateral nuclei of the amygdala. Supported by MH 54557 to J.W.G and M.W.M.
Society for Neuroscience Abstracts, 24 (1998), 1901.