The effect of stimulation of peripheral and supraspinal sensory system on the activities of raphe-spinal neurons were studied extracellularly in chloralose-anesthetized cats. Among 300 raphe neurons recorded from the brainstem of cats, a total of 74 raphe-spinal neurons were activated antidromically by stimulation of the cervical dorsolateral funiculus. The mean conduction velocity of these neurons, calculated from the stimulation-recording distance and latencies, was 25.4 m/sec.
These raphe-spinal neurons were found to originate in the caudal raphe nuclei,
i.e., 56 in raphe magnus, 14 in raphe obscurus, 3 in raphe pallidus and 1 in raphe pontis. All of them were shown to respond to innocuous and/or noxious peripheral mechanical stimuli, all with broad receptive fields. Single pulse periaqueductal gray (PAG) stimulation evoked driven firing with the spike per stimulus ratio ranging from 1 to 4 and latencies ranging from 5 to 15 msec in 57 (95%) of 60 units examined. Driven firing was followed by inhibition with a period ranging from 100 to 200 msec. Repetitive PAG stimulation at 20 Hz induced powerful facilitation of firing. The facilitation persisted for several minutes after termination of the stimulation when the repetitive stimulation was continued for 5 to 30 sec.
Single pulse VPL or VPM stimulation evoked driven firing with the spike per stimulus ratio ranging from 1 to 4 and latencies ranging from 10 to 20 msec in 58 (97%) of 60 units tested. Long lasting powerful facilitation was also provoked in those units by repetitive stimulation at 20 Hz for 5 to 30 sec. This facilitation was not affected by removal of the bilateral sensorimotor area.
PAG-induced facilitation was apparently and reversibly avoided by the administration of naloxone (0.1-0.3 mg/kg, i.v.) in 7 (70%) of 10 units investigated. On the other hand, the administration of naloxone (0.3 mg/kg, i.v.) was found not to affect VPL-induced facilitation of firing in any of ten units examined.
Effects of sustained repetitive stimulation of the thalamic relay nucleus on activities of raphe-spinal neurons were studied in 17 units. After sustained stimulation for 3 hours, facilitation of firing by the thalamic relay nucleus stimulation was shown to completely disappear. Facilitatory response to single pulse thalamic relay nucleus stimulation was also found to be reduced. Nevertheless, facilitation of firing induced by single pulse or repetitive PAG stimulation was apparently unchanged.
These results suggest that both thalamic relay nucleus stimulation and PAG stimulation for pain-relief may activate a final common path,
i.e., raphe-spinal neurons, which then inhibit spinal neurons sensitive to pain, as a part of the mechanism of pain-suppression. Although the thalamic relay nucleus-induced facilitation of raphe-spinal neurons was shown to be as powerful as that of PAG, it did not appear to relate to the opiate mechanism, unlike that of PAG.
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