SHOCK-INDUCED HYPERALGESIA IN RATS: EVIDENCE THE DORSOLATERAL PERIAQUEDUCTAL GRAY IS NECESSARY BUT NOT SUFFICIENT. A. N. Sieve *, G. Garcia, E. D. Crown, J. W. Grau, and M. W. Meagher. Dept. of Psychology, Texas A&M Univ., College Station, TX 77843

Prior studies have shown that the dorsolateral periaqueductal gray (dlPAG) is involved in some forms of environmentally-induced hyperalgesia. Lesions of the dlPAG have been shown to eliminate the behavioral consequences of moderate tailshock (3, .75 sec, 1 mA) that are indicative of hyperalgesia: decreases in vocalization thresholds to heat and shock, and enhancement of learning about an aversive stimulus (conditioned freezing to a weak shock) (McLemore, et al, Beh. Neuro., 1999).

This study sought to further elucidate the neurochemical system in the dlPAG involved in the induction of hyperalgesia. Chemically inactivating the dlPAG by microinjecting the GABA(A) agonist midazolam blocked shock-induced hyperalgesia. However, indirectly activating the dlPAG by microinjecting the GABA antagonist bicuculline did not induce hyperalgesia. Instead, hypoalgesia was observed. Hypoalgesia was also observed in response to direct activation of the dlPAG glutamate system with kainic acid. Thus, activation of the same neurochemical system necessary for hyperalgesia, was not sufficient to induce hyperlagesia. Supported by MH54557 to J. W. G. and M. W. M.

Society for Neuroscience Abstracts, 26 (2000), 653.

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