Two different experimental procedures have been utilized to study the possible role of midbrain raphe neurons in mediating the increase in brain 5-HT catabolism induced by an elevated ambient temperature. In one experimental series, lesions were placed in the midbrain raphe nuclei to evaluate the importance of the perikarya of 5-HT containing neurons in mediating the heat-induced increase in the 5-HT metabolite, 5-HIAA. THe raphe lesions were made 3 h prior to a period of incubation of 40° C; upon completion of the incubation period, the forebrain, which is the principal projection area of the midbrain raphe neurons, was assayed for 5-HIAA. Lesions destroying a large portion of the midbrain raphe nuclei were found to completely prevent the heat-induced increase in brain 5-HIAA concentration. Lesions made outside the midbrain raphe nuclei did not prevent the rise in 5-HIAA. In another set of experiments the rate of firing of single units in the raphe nuclei was monitored while rats were exposed to infrared radiation in order to determine if a rise in body temperature is associated with an altered rate of firing of the serotonin-containing neurons in the midbrain. It was found that as body temperatures rises there is a concomitant increase in the rate of firing of individual raphe neurons. Under these conditions the firing of raphe units can be entirely inhibited by LSD. Neurons located outside the raphe nuclei (pons; reticular formation) do not show any obvious correlation between rate of firing and body temperatures and are not inhibited by LSD. It is hypothesized that changes in forebrain 5-HIAA concentration induced by elevated ambient temperatures are mediated at least in part by an increased rate of firing of the 5-HT cotaining neurons. © 1971.
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