LESIONS OF TE FRONTAL CORTEX ATTENUATE THE ANALGESIA OBSERVED AFTER VERY BRIEF BUT NOT LONG SHOCKS. J.W. Grau and M.W. Meagher. Dept. of Psychology, Texas A&M University, College Station, Texas 77843 and Dept. of Psychology, University of North Carolina, Chapel Hill, NC 27514.
Considerable evidence exists that neural systems in the brainstem can modulate the flow of nociceptive information at the level of the spinal cord. Elsewhere we investigated whether neural systems in the forebrain play a role in activating these brainstem systems (see the abstract by M.W. Meagher and J.W. Grau). We showed that decerebration blocks the analgesia observed after very brief shocks, which suggests that forebrain sstems mediate the activation of the analgesic systems in this situation. By contrast, decerebration potentiated the analgesia observed after long shocks. This suggests that long shocks can also directly activate the analgesic systems in the brainstem, and if anything, neural systems in the forebrain may inhibit the direct activation of the analgesic systems by long shock. The present study assesses whether lesions of the frontal cortex would have a similar impact on the analgesia observed after very brief or long shocks.
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 received lesions of the frontal cortex. The subjects were then tested 24 to 30 hr later. The subjects were placed in restraining tubes and allowed to acclimate for 15 min. Baseline pain reactivity was then assessed with the tail-flick test. 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 differences existed between the groups prior to shock exposure. Both the brief and the long shocks induced significant analgesia in the sham controls. In lesioned subjects exposure to brief shocks did not induce analgesia. By contrast, exposure to long shocks induced a strong analgesia. However, unlike decerebration, lesions of the frontal cortex did not potentiate this analgesia.
These findings suggest that neural systems within the frontal cortex play a critical role in mediating tha anlagesia observed after very brief shocks. This finding is of particular interest sinsce others have shown that electrical stimulation of cells in this region can elicit analgesia on the tail-flick test (e.g. Hardy, S.G.P., Brain Rsch, 339:281, 1985). The fact that lesions of the frontal cortex did not affect the analgesia observed after long shocks suggests that neural systems in this region may not play a role in modulating the direct activation of the analgesic systems.
Published in Society for Neuroscience Abstracts, 13, 1987.