EFFECTS OF AMINOPYRINE AND PHENYLBUTAZONE ON THE ACTIVITY OF NEURONS IN THE TRIGEMINAL NUCLEI AND HYPOTHALAMUS

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Informations for the neural mechanism of pain sensation are still insufficient. Haugen and Melzack (1, 2) have shown that the afferent fibers most closely related to pain perception caused by electrical stimulation of the tooth pulp project to the sensory cortex through the trigemino-bulbo-thalamic tract, but not via the trigeminal lemniscus. The significance of participation of the thalamic intralaminal nuclei in pain mechanism has been emphasized by Gangloff and Monnier (3) and Albe-Fessard and Kruger (4). However, the concept of a specific pain center in the brain is considered to be totally inadequate, since the thalamus, hypothalamus, brainstem reticular formation and parietal cortex are all implicated in pain perception (5). In the previous paper (6), it was presumed that 1) the hypothalamus formed closed circuits with other brain structures, and 2) the circulation of impulses within these circuits might contribute to the central regulation of sensory mechanism. In the present experiments, the effects of aminopyrine and phenylbutazone on the evoked potentials in the sensory cortex and posterior hypothalamus as well as on the responses of unit discharges in the posterior hypothalamus and trigeminal nuclei to afferent electrical stimulation of the inferior alveolar nerve were studied in attempt to find the mode of action of these analgesics in the central nervous system.
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