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J Auton Nerv Syst. 1987 Jan;18(1):61-72.

Inhibition of cardiopulmonary input to thoracic spinothalamic tract cells by stimulation of the subcoeruleus-parabrachial region in the primate.


Effects of electrically stimulating the subcoeruleus-parabrachial (SC-PB) region on 31 spinothalamic tract neurons which receive excitatory input from cardiopulmonary sympathetic afferent fibers were studied in 21 monkeys anesthetized with chloralose. A conditioning stimulus to the SC-PB region inhibited the activity of 5 cells responding to the test stimulus applied to sympathetic afferent fibers. At a conditioning-test interval of 10 ms, test responses were maximally reduced to 47 +/- 6% of the control. Inhibitory effects were present at conditioning-test intervals up to 150 ms. Excitatory effects of both A delta-and C-fiber sympathetic afferents were reduced by stimulation of the SC-PB region; however, C-fiber input was more powerfully inhibited. Intracardiac injection of the algesic agent bradykinin excited 8 of 12 spinothalamic tract neurons tested; the responding cells increased their activity from 12 +/- 13 to 31 +/- 8 impulses/s. SC-PB stimulation (212 +/- 45 microA) reduced the peak activity caused by bradykinin to 6 +/- 2 impulses/s. Aortic occlusion increased the discharge rate of 5 out of 8 neurons from 13 +/- 3 to 21 +/- 4 impulses/s. At the peak of the response of aortic occlusion, SC-PB stimulation (238 +/- 20 microA) decreased neuron activity to 3 +/- 0 impulses/s. Effective sites for inhibition of spinothalamic tract cell activity were located in the lateral and medial parabrachial nuclei and the nucleus subcoeruleus. This study demonstrates that stimulation of the dorsolateral pons can inhibit the responses of upper thoracic spinothalamic tract neurons to cardiopulmonary sympathetic afferent input. Our laboratory previously has shown that stimulation of cardiopulmonary vagal afferents inhibits spinothalamic tract cells via supraspinal mechanisms. The SC-PB region may be a site activated by cardiac vagal afferents during ischemia and therefore, may be involved in the etiology of painless myocardial infarctions.

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