PREVIOUSLY FOOD DEPRIVED RATS EXHIBIT A NALTREXONE REVERSIBLE INCREASE IN BOTH REACTIVITY TO SHOCK AND SHOCK-INDUCED ANALGESIA. P.A. Illich & J.W. Grau. Dept. of Psychology, Texas A&M University, College Station, TX 77843.
Prior work has shown that exposure to uncontrollable shock elicits a strong, hormonally mediated, opioid analgesia (Terman et al., Science, 226:1271, 1984). In addition, it sensitizes subjects to becoming analgesic 24 hrs later upon exposure to mild shock (Grau et al., Science, 203:1409, 1981). Here we assess the impact of another manipulation that elicits a hormonally mediated opioid analgesia, food deprivation (Hamm et al., Physiol. & Beh., 35:879, 1985). After 2 days of baseline testing, deprived subjects had their food removed. At the end of day 3, they received 9 grams of food. Food was returned on day 4. Contrary to other reports, food deprivation per se did not induce a significant analgesia. On day 5, 24 hrs after food was returned, we assessed the impact of mild shock (3, 0.75-sec, 1-mA). Interestingly the subjects who had been previously food deprived vocalized and strained significantly more to the mild shock. Oddly, this heightened reactivity was blocked by naltrexone. After the last shock, pain reactivity was assessed with the tail-flick test. Previously food deprived subjects exhibited a potentiated analgesia. This effect too was attenuated by naltrexone.
Published in Society for Neuroscience Abstracts, 15, 1989.