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  • Title: Raphe magnus inhibition of primate T1-T4 spinothalamic cells with cardiopulmonary visceral input.
    Author: Ammons WS, Blair RW, Foreman RD.
    Journal: Pain; 1984 Nov; 20(3):247-260. PubMed ID: 6514373.
    Abstract:
    Effects of stimulation of nucleus raphe magnus on upper thoracic spinothalamic tract neurons were determined. Experiments were performed on 15 monkeys (Macaca fascicularis) anesthetized with alpha-chloralose. Forty-two T1-T4 spinothalamic tract neurons with viscerosomatic inputs were studied. Stimulation of nucleus raphe magnus inhibited activity of all 42 neurons. Thirty-two of these cells had background activity. The magnitude of the inhibition of background activity was related to the raphe magnus stimulus current. Current strengths as low as 300 microA (100 Hz, 0.2 msec duration) completely inhibited most cells. Current thresholds averaged 80 +/- 10 microA and were unrelated to the type of somatic or visceral input the cell received, or to the cell location. Conditioning stimuli applied to nucleus raphe magnus inhibited cell responses to electrical stimulation of cardiopulmonary sympathetic A delta and C afferent fibers. However, in order to demonstrate preferential inhibition of responses to C fiber input it was necessary to use 200 msec trains of raphe stimuli which were concurrent with the cell response to sympathetic afferent stimuli. Twenty-five spinothalamic neurons were tested for responses to intracardiac injections of bradykinin and 17 cells increased their discharge rate. Stimulation of nucleus raphe magnus (280 +/- 25 microA) near the peak of the response reduced activity of all 17 cells from 26 +/- 3 to 4 +/- 1 spikes/sec (P less than 0.001). Raphe stimulation inhibited responses of 41 of 41 cells to noxious pinch and responses of 15 of 15 wide dynamic range and the 1 low threshold cell to blowing hair. The results establish the capacity of the raphe-spinal pathway to modulate activity of upper thoracic spinothalamic tract neurons including their response to potentially noxious cardiac stimuli. It is therefore possible that descending inhibitory systems may modulate ascending information related to cardiac pain and perhaps account for myocardial ischemic attacks which occur without pain.
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