DECERBRATION BLOCKS THE ANALGESIA OBSERVED AFTER VERY BRIEF BUT NOT LONG SHOCKS. M.W. Meagher and J.W. Grau. Dept. of Psychology, UNC, Chapel Hill, NC 27514 and Dept. of Psychology, Texas A&M University, College Station, Texas 77843.

We have suggested that the memory of an aversive event may activate the brainstem systems which modulate the flow of nociceptive information at the level of the spinal cord (Grau, J.W., Beh. Neurosci., 101:272, 1987). Supporting this hypothesis, we have shown that factors which should speed the decay of the memory also speed the decay of analgesia. On the basis of this behavioral evidence we have suggested that forebrain systems may mediate the activation of the analgesic systems when an organism is exposed to mild aversive events. By contrast, others (e.g. Watkins, L.R. et al., Brain Rsch., 276:317, 1983) have suggested that the analgesic systems may be directly activated at the level of the brainstem and that forebrain systems are not essential. Supporting this notion, they have shown that decerebration has little impact on the magnitude of shock indeced analgesia. However, the duration of shock exposure employed in these studies (90 sec) is considerably longer than the shock duration (2.25 sec) we typically use. Thus, it is possible that forebrain systems do mediate the analgesia observed after very brief shocks, whereas long shocks may directly activate the brainstem analgesic systems. The present experiment tests this hypothesis.

The subjects were 48 male Sprague-Dawley rats (100-120 days old). One-half of the subjects experienced sham surgery under Pentothal anaesthesia. The other half receivedmid-collicular decerebrations. Eight to ten hr later the subjects were placed in restraining tubes and allowed to acclimate for 15 min. Baseline pain reactivity was then assessed. One third of the subjects then received 3 very brief (0.75) 1.0 mA shocks spaced 20 sec apart. Another third received 3 long (25 sec) 1.0 mA shocks spaced 20 sec apart. The remaining subjects served as unshocked controls. Five tail-flick tests were then administered at 2 min intervals.

No significant difference existed between the groups prior to shock exposure. Both the very brief shocks and the long shocks induced significant analgesia in the sham controls. However, the very brief shocks did not induce analgesia in decerebrate subjects. By contrast, exposure to long shocks did induce a strong analgesia. In fact, exposure to long shocks did induce a strong analgesia. In decerebrate subjects than it did in the sham controls.

This study shows that forebrain systems mediate the activation of the analgesic systems when subjects are exposed to very brief shocks. it also shows that long shocks are capable of directly activating the brainstem analgesic systems. The fact that decerebration potentiated this analgesia suggests that forebrain systems may actually inhibit the direct activation of the analgesic systems by long shocks.

Published in Society for Neuroscience Abstracts, 13, 1987.

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