1. Lumbosacral spinothalamic tract (STT) neurons can be inhibited by noxious pinch of the contralateral hindlimb or either forelimb and by electrical stimulation of cardiopulmonary sympathetic, splanchnic, and hypogastric afferents. A previous study found that spinal transections between C2 and C4 sometimes abolished the inhibitory effect of spinal afferent input and sometimes left it intact. This suggested that propriospinal neurons in the C1 and C2 segments might mediate this effect. To test whether neurons in the C1 and C2 segments were involved in producing this inhibitory effect, the magnitude of the reduction in neural activity was measured in the same STT neuron before and after spinal transection at C1 or between C3 and C7. 2. All neurons were antidromically activated from the contralateral thalamus and thoracic spinal cord. For us to accept a neuron for analysis, the characteristics of the somatic input and the latency and shape of the antidromatic spike produced by spinal cord stimulation had to be the same before and after the spinal transection. Also, spinal transection often causes a marked increase in spontaneous cell activity, which may affect the magnitude of an inhibitory response. To avoid this confounding problem, a cell was accepted for analysis only if it showed marked inhibition of high cell activity evoked by somatic pinch before spinal transection. For analysis 13 STT neurons met these criteria: 6 neurons were in monkeys with C1 transections, and 7 neurons were in animals with transections between C3 and C7.(ABSTRACT TRUNCATED AT 250 WORDS)

1. Extracellular recordings were made from 41 spinothalamic tract (STT) neurons on the left side of the T2-T5 spinal segments of 20 monkeys (Macaca fascicularis) anesthetized with alpha-chloralose. Manipulation of the left triceps-chest region and electrical stimulation of cardiopulmonary sympathetic afferent fibers excited these cells. 2. Isotonic urinary bladder distensions (UBD) to pressures between 20 and 80 cmH2O reduced the spontaneous activity in 33 of 41 cells. Cell activity was significantly reduced by UBD at 20 cmH2O. Distensions to 40, 60, and 80 cmH2O produced progressively greater reductions in spontaneous discharge. Activity was decreased throughout distension in 29 cells (tonic inhibition) and at the onset of distension in 3 neurons (phasic inhibition). In one cell, inhibition followed a brief excitation at the onset of distension (phasic excitation-tonic inhibition). Spontaneous bladder contractions also inhibited STT cell activity. 3. Inhibition by UBD was observed in STT cells characterized as wide dynamic range, high threshold, and high threshold inhibitory. No correlation existed between cell type or laminar location and inhibition by urinary bladder distension. Cells excited by cardiopulmonary sympathetic afferent A delta- and C-fibers had a significantly greater tendency to be inhibited by UBD (17 of 18) than cells activated by A delta- but not C-fibers (13 of 20). 4. Urinary bladder distension and pinch of the hindlimbs also reduced activity of STT cells excited by input from cardiopulmonary sympathetic afferents and from the proximal forelimb. 5. Urinary bladder distension to 40, 60, or 80 cmH2O produced a greater absolute but smaller relative reduction in the firing frequency of STT cells as spontaneous activity increased. Thus the magnitude of this inhibitory effect may depend on whether the inhibitory effect is measured as an absolute or relative change in cell activity. 6. Convergent inhibitory input from somatic regions also was observed. Noxious pinch of the hamstring region of the right hindlimb decreased activity in 32 of 39 cells. Left hindlimb pinch inhibited 21 of 38 cells, and 15 of 29 cells were inhibited by right triceps pinch. 7. Convergent inhibitory input from the hamstring region of the hindlimbs and from the urinary bladder to upper thoracic STT cells may be important for coding the intensity and location of noxious visceral and somatic stimuli and for organizing the appropriate sequence of motor responses when multiple noxious stimuli are present.

Effects of electrically stimulating vagal afferents were determined on lumbosacral spinothalamic tract (STT) neurons in the T9-S1 segments. Stimulating left or right vagal afferents inhibited 20 (50%) and excited 4 (10%) of 40 STT neurons. Vagal stimulation reduced activity of the 20 inhibited cells by 71 +/- 6% and reduced the average activity of all 40 STT neurons by 28% from 11.5 +/- 1.3 to 8.3 +/- 1.4 impulses/s (P less than 0.01). Effects of activating thoracic and abdominal or just abdominal vagal afferents were also determined. Stimulating right abdominal vagal afferents inhibited 4 (11%), excited 1 (3%), and did not affect 30 (86%) of the STT neurons and overall did not significantly affect STT cell activity. In contrast, in 33 of these cells stimulation of afferents in the right cervical vagus inhibited 16 (48%), excited 2 (6%), and did not affect 15 (45%) neurons and overall significantly reduced cell activity by 29% (P less than 0.01). These data and those of Ammons et al. (J. Neurophysiol. 50: 926-940, 1983; Circ Res. 53: 603-612, 1983; J. Neurophysiol. 54: 73-89, 1985) suggest that cardiopulmonary but not abdominal vagal afferent input reduces STT cell activity in many spinal segments. This inhibitory vagal reflex may play a role in protecting the heart.

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.