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Biomedical subjects

R D Foreman

Publications and source records attributed to R D Foreman.

At least 91 records · Page 5Linked to original sources
PubMed1985

Effects of intracardiac bradykinin on T2-T5 medial spinothalamic cells.

Effects of injecting bradykinin (2 micrograms/kg) into the left atrium on spinothalamic tract neurons projecting to medial thalamus (M-STT cells), to the ventral posterior lateral nucleus of the thalamus (L-STT cells), or to both (LM-STT cells) were examined in 18 monkeys (Macaca fascicularis) anesthetized with alpha-chloralose. Bradykinin increased cell activity in 11/16 M-STT cells, 10/15 L-STT cells, and 4/7 LM-STT cells. One M-STT cell was inhibited. Peak responses to bradykinin of the three cell groups were not different. LM-STT cells began to respond and reached peak responses slightly earlier than the other two groups. Six M-STT, four L-STT, and two LM-STT cells became entrained to the cardiac cycle during their responses to bradykinin. Responses to bradykinin were not dependent on the type of somatic input or cell location. Responding cells most often received A delta- and C-fiber sympathetic input, but some responding cells had only A delta-input. These results demonstrate that in addition to L-STT cells STT cells projecting to the medial thalamus respond to a potentially noxious cardiac stimulus. These cells may participate in the motivational-affective component of cardiac pain.

Action Potentials↗
PubMed1985

Raphe magnus inhibition of feline T1-T4 spinoreticular tract cell responses to visceral and somatic inputs.

Background activity of spinoreticular tract neurons in the T1-T4 segments was on average inhibited 80% by electrical stimulation of nucleus raphe magnus. Nucleus raphe magnus stimulation inhibited responses of spinoreticular tract neurons to somatic input produced by touching the skin and hair (innocuous stimulus) or pinching the skin and muscle (noxious stimulus). Inhibition of responses to noxious and innocuous somatic inputs was not significantly different. Inhibition produced during nucleus raphe magnus stimulation was less effective when the activity of spinoreticular tract cells increased. This relationship was consistent for both background activity and responses to somatic noxious or innocuous input. Nucleus raphe magnus stimulation inhibited responses of spinoreticular tract neurons to visceral input produced by electrical stimulation of cardiopulmonary sympathetic afferent fibers. Responses to C-fiber sympathetic afferent fibers were more effectively inhibited than were responses to A-delta sympathetic afferent fibers. In conclusion, stimulation of the nucleus raphe magnus inhibits T1-T4 spinoreticular tract neuronal responses to visceral and somatic inputs. Since spinoreticular neurons project to the medullary reticular formation, activation of the nucleus raphe magnus could modulate affective-motivational behavior and cardiovascular adjustments that often occur during angina pectoris.

Animals↗
PubMed1985

T2-T5 spinothalamic neurons projecting to medial thalamus with viscerosomatic input.

Spinothalamic tract neurons projecting to medial thalamus (M-STT cells), ventral posterior lateral nucleus (VPL) of the thalamus (L-STT cells), or both thalamic regions (LM-STT cells) were studied in 19 monkeys anesthetized with alpha-chloralose. Twenty-seven M-STT cells were antidromically activated from nucleus centralis lateralis, nucleus centrum medianum, or the medial dorsal nucleus. Stimulation of VPL elicited antidromic responses from 22 cells and 13 cells were activated from both VPL and medial thalamus. Antidromic conduction velocities of M-STT cells were significantly slower than those of L-STT or LM-STT cells. M-STT cells were located in laminae I, IV, V, and VII with greater numbers found in the deepest laminae. L-STT cells were located mostly in lamina IV, whereas most LM-STT cells were found in lamina V. Twenty-four of 27 M-STT cells, all L-STT cells, and all LM-STT cells received input from both cardiopulmonary sympathetic and somatic afferent fibers. WDR cells were most common among the L-STT and LM-STT groups, whereas HT cells were the most common class in the M-STT cell group. Excitatory receptive fields of M-STT cells were large, and often bilateral. Receptive fields of L-STT cells were simple and never bilateral. Receptive fields of LM-STT cells could be similar to M-STT or L-STT cells. Thirty-three percent of the M-STT cells, 37% of the L-STT cells, and 62% of the LM-STT cells had inhibitory receptive fields. Inhibition was elicited most often by a noxious pinch of the hindlimbs. Sixteen of 23 (70%) M-STT cells received C-fiber cardiopulmonary sympathetic input in addition to A-delta-fiber input. The other 7 cells received only A-delta-fiber input. Only 45% of the L-STT cells and 38% of the LM-STT cells received both A-delta- and C-fiber inputs. The maximum number of spikes elicited by A-delta-input was related to segmental locations for L-STT cells with greatest responses in T2 and lesser responses in more caudal segments; however, no such trend was apparent for M-STT cells or for responses to C-fiber input for either group. Electrical stimulation of the left thoracic vagus nerve inhibited 7 of 18 M-STT cells, 10 of 16 L-STT cells, and 6 of 12 LM-STT cells. These results are the first description of visceral input to cells projecting to medial thalamus.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1985

Neural regulation of the cardiovascular system during exercise.

Neural components important in control of the cardiovascular system during exercise can be divided into central nervous system (CNS) components and peripheral components. CNS components would include the cerebral cortex, cerebellum, medullary region of the brain stem, and the spinal cord. Peripheral components would include the efferent limbs of the autonomic nervous system and afferent fibers carrying information to the CNS. The neural pathways involved in the control of cardiovascular system during exercise and the relationship between the various neural components have been actively pursued in the last few years. Several new studies suggest that information arising from the active muscles and the cardiovascular system itself may be important in the control of the cardiovascular system during exercise. The cerebellum may play a modulating role in the cardiovascular response. The information from the peripheral afferent fibers, the cerebellum, and the cerebral cortex is integrated in the brain to result in overall neural control. Exercise training probably modifies the central integration of information and modifies the cardiovascular response to exercise and other stresses.

Afferent Pathways↗
PubMed1984

Cardiovascular and T2-T4 dorsal horn cell responses to gallbladder distention in the cat.

Effects of gallbladder distention on blood pressure, heart rate, and T2-T4 dorsal horn cell activity were determined in 18 cats anesthetized with alpha-chloralose. Distention of the gallbladder (10-100 mm Hg) increased blood pressure in 17 of 18 cats, but heart rate was altered in only 2. The gallbladder pressure-blood pressure relation was derived for 11 cats. Pressor responses were greater with greater distending pressures over the gallbladder pressure range of 20-80 mm Hg. The maximum increase in blood pressure was 21 +/- 6 mm Hg at a gallbladder pressure of 80 mm Hg. Effects of gallbladder distention were tested on 64 T2-T4 dorsal horn neurons which met the following criteria: they had a somatic receptive field and were excited or inhibited by electrical stimulation of the left greater splanchnic nerve. In addition, all 64 neurons responded to stimulation of cardiopulmonary sympathetic afferent fibers. Gallbladder distention excited 17 cells and inhibited 9 cells. Responses usually consisted of phasic and tonic components. Significant increases or decreases in cell activity were elicited at a gallbladder pressure of 40 mm Hg. Pressor responses as well as changes in cell activity were abolished or greatly attenuated when both greater splanchnic nerves were sectioned. Vagotomy had no effect. Gallbladder pressure thresholds for a change in blood pressure (27 +/- 3 mm Hg) and cell activity (29 +/- 4 mm Hg) were not significantly different. Cells responding to gallbladder distention were located in laminae IV-VII of the T2-T4 segments. We conclude that gallbladder distention alters cell activity in the upper thoracic spinal cord and increases blood pressure. These findings may explain the phenomenon of chest pain which results from disease of the gallbladder.

Angina Pectoris↗
PubMed1984

Viscerosomatic convergence onto T2-T4 spinoreticular, spinoreticular-spinothalamic, and spinothalamic tract neurons in the cat.

Neurons of T2 to T4 spinal segments were antidromically activated from the medullary reticular formation and the contralateral region in or near the ventral posterior lateral nucleus of the thalamus. Sixty-seven percent of the spinoreticular neurons projected to the ipsilateral, contralateral, or both ipsilateral and contralateral medullary reticular formation. In addition, 21% of the cells projected to the reticular formation and thalamus and 12% projected only to the thalamus. These cells received both visceral and somatic inputs. Electrical stimulation of cardiopulmonary sympathetic afferent fibers elicited an early peak of cell activity in 30 cells, an early and late peak in 38 cells, and only a late peak in 1 cell. Seventy-one percent of the cells had simple somatic receptive fields; these fields were localized to the left forelimb and left upper thorax. The remaining 29% of the cells had complex receptive fields that often extended to the hind limb as well as bilaterally. Classification of all cells according to threshold for activation of the somatic receptive field showed that 86% of the cells were high-threshold, 10% were wide dynamic range, and 4% were high-threshold but, in addition, were inhibited during hair movement. Viscerosomatic convergence onto these cells support Ruch's convergence projection theory for referred pain. These projecting neurons may be involved with referred pain associated with angina pectoris. In addition, they may also be involved with cardiovascular adjustments.

Animals↗
PubMed1984

Raphe magnus inhibition of primate T1-T4 spinothalamic cells with cardiopulmonary visceral input.

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.

Animals↗
PubMed1984

Fastigial nucleus projections to the brain stem in beagles: pathways for autonomic regulation.

Efferent connections from a portion of the cerebellar fastigial nucleus were investigated using autoradiography. Bipolar stimulating electrodes were placed in the fastigial nucleus of anesthetized beagles and the area that produced increases in blood pressure and heart rate was localized. A mixture of [3H]leucine and [3H]proline (4:1) was injected into the area and autoradiograms of transported material were prepared. Injections filled the rostral and various parts of the caudal fastigial nucleus. Labeled axons reached the brain stem via two routes, the ipsilateral juxtarestiform body and the contralateral uncinate fasciculus. Ventral portions of the lateral vestibular nucleus were labeled bilaterally, projections to the inferior vestibular and medial vestibular nuclei are contralateral. Nucleus tractus solitarius was heavily labeled on the side opposite the injection. The contralateral medial reticular formation contained many labeled terminals and axons. Label was found in the nucleus reticularis ventralis, lateral reticular nucleus, nucleus gigantocellularis, nucleus pontis caudalis and the paramedian reticular nucleus. No terminal labeling was found in nucleus parvocellularis or nucleus ambiguous. Stimulation of the rostral fastigial nucleus produces increases in blood pressure and heart rate by generalized sympathoexcitation. Many cell groups which facilitate the activity of preganglionic sympathetic neurons do not receive direct fastigial input. It is suggested that that sympathoexcitation resulting from stimulation of the fastigial nucleus occurs through multisynaptic connections in the brain stem.

Animals↗
PubMed1984

Responses of T2-T4 spinal neurons to stimulation of the greater splanchnic nerves of the cat.

Effects of electrical stimulation of the greater splanchnic nerves on T2-T4 spinal neurons were determined in 16 cats anesthetized with alpha-chloralose. Of 77 neurons responding to somatic stimuli, 65 (84%) were excited, inhibited, or both excited and inhibited by splanchnic input. Each of the splanchnic responsive cells also was responsive to electrical stimulation of cardiopulmonary sympathetic afferent fibers. All but one neuron with left splanchnic input also received input from the right splanchnic nerve. Short- and long-latency excitatory responses were observed after splanchnic stimulation. The cell response to splanchnic stimulation was greatly inhibited by a conditioning stimulus applied to the other splanchnic nerve. A similar, although weaker, interaction occurred between splanchnic and cardiopulmonary sympathetic afferent fibers. The activity of 17 cells was inhibited by repetitive stimuli applied to one or both splanchnic nerves. Cells were found in laminae I, IV, V, VII, and VIII. These data provide the first evidence for splanchnic modulation of upper thoracic dorsal horn neurons.

Afferent Pathways↗
PubMed1984

Responses of thoracic spinoreticular and spinothalamic cells to intracardiac bradykinin.

The response characteristics of spinoreticular and spinothalamic cells to intracardiac injection of bradykinin were determined in cats anesthetized with chloralose. Extracellular potentials of individual spinoreticular and spinothalamic cells were recorded from the T2-T4 segments of the spinal cord. Only those cells with cardiopulmonary sympathetic afferent input were tested for responses to intracardiac bradykinin (1-6 micrograms/kg). Thirty-seven of the 64 cells studied responded to bradykinin; 36 were excited and one was inhibited. For excited cells, discharge rate increased from 4 +/- 1.0 (SE) spikes/s to a peak of 20 +/- 2.4 spikes/s, a fivefold increase. Latency to onset of cell response was 13 +/- 1.1 s, and latency to peak response was 24 +/- 1.4 s after drug injection. Tachyphylaxis to additional doses of bradykinin was observed in 17 of 32 cells. Occurrence of tachyphylaxis was sometimes altered after bilateral cervical vagotomy. The projection sites in the caudal medulla and thalamus were similar for responsive and nonresponsive cells. Laminar cell locations in the spinal cord had no significant influence on likelihood of cell response to bradykinin. We conclude that spinoreticular and spinothalamic cells have a role in transmitting noxious information from the heart to the brain.

Animals↗
PubMed1984

Responses of primate T1-T5 spinothalamic neurons to gallbladder distension.

Extracellular unit recordings were obtained from 44 spinothalamic tract (STT) neurons in the T1-T5 segments of 15 alpha-chloralose anesthesized monkeys (Macaca fascicularis). Each cell had a somatic receptive field in the left chest region and was excited by electrical stimulation of cardiopulmonary sympathetic afferent fibers. Gallbladder distension to pressures between 20 and 100 mmHg increased activity in 16 of 44 neurons. Responses usually consisted of bursts of activity associated with increased gallbladder pressure (phasic responses) followed by maintained activity during the distension (tonic responses). Magnitude of phasic responses was linearly related to the distending pressure and was consistently greater than magnitude of tonic responses. The gallbladder-responsive and nonresponsive groups included similar proportions of wide dynamic range, high threshold, and high-threshold inhibitory cells. Nine of 10 gallbladder-responsive cells and 11 of 21 gallbladder-nonresponsive cells increased their discharge rate after injection of 2 micrograms/kg bradykinin into left atrium. Activity of cells with gallbladder input increased from 14 +/- 4 to 33 +/- 4 spikes/s. Cells without gallbladder input increased their discharge rate to a significantly less degree (10 +/- 3-23 +/- 4 spikes/s). These results indicate that upper thoracic STT neurons may increase their activity during gallbladder distension. Convergence of afferent information from the chest and gallbladder may explain chest pain occurring during gallbladder disease. Furthermore the tendency of gallbladder-responsive cells to respond to bradykinin injections with a high rate of discharge could explain how this chest pain of gallbladder origin may closely mimic pain of angina pectoris.

Angina Pectoris↗
PubMed1984

Greater splanchnic excitation of primate T1-T5 spinothalamic neurons.

Effects of electrical stimulation of the left greater splanchnic nerve (SPL) on T1-T5 spinothalamic (STT) neurons were determined. Eighty-five STT neurons were studied in 36 anesthetized monkeys (Macaca fascicularis). All neurons were excited by manipulation of their somatic receptive fields and by electrical stimulation of cardiopulmonary (CP) sympathetic afferent fibers. SPL stimulation excited 63 (74%) STT neurons. There was an increasing percentage of cells with SPL input at more caudal segments and in deeper laminae. Both SPL and CP sympathetic stimulation elicited early or both early and late responses. Latencies to cell activation were usually shorter for CP sympathetic stimulation than for SPL stimulation (5.4 +/- 0.8 versus 11.3 +/- 2.0 ms for early responses and 44.2 +/- 4.2 versus 111.0 +/- 6.6 ms for late responses). The maximum number of spikes per SPL or CP sympathetic stimulus was determined. In the T2 and T3 segments, early responses to CP sympathetic stimulation were significantly greater. However, at more caudal segments, responses to CP sympathetic input decreased while responses to SPL input increased until at T4 there was no difference in the two responses. In T5, responses to SPL input were greater. No differences in the magnitudes of late responses were observed in any of the segments. The response of six cells to SPL stimulation was inhibited by a train of conditioning stimuli applied to the left thoracic vagus nerve. Maximum inhibition occurred at a CT interval of 50 ms and test responses were significantly reduced at CT intervals as great as 200 ms. Bilateral vagotomy eliminated the inhibitory effect. Cutting the left sympathetic chain between the T5 and T6 rami communicantes eliminated 27% of the response to SPL stimulation. More caudal cuts reduced the response further until 71% of the response was abolished by a cut between T8 and T9. Lesions in the dorsolateral column of the spinal cord had little effect on the responses, while lesions of the lateral and ventrolateral columns reduced or abolished the responses. We conclude that SPL stimulation excites T1-T5 STT neurons by way of extraspinal and intraspinal pathways. SPL information is integrated with information from a variety of other visceral and somatic sources. SPL input to cells with somatic fields in the chest region may explain the clinical phenomenon of chest pain associated with abdominal disorders.

Animals↗
PubMed1984

Responses of thoracic spinothalamic and spinoreticular cells to coronary artery occlusion.

Spinothalamic and spinoreticular neurons in the C8-T5 spinal segments were examined for responsiveness to occlusion of the left main, left circumflex (CX), or left anterior descending (LAD) coronary artery in monkeys and cats. Four types of cell response to occlusion were observed, as follows: 1) cell activity increased (6 responses) or decreased (1 response) to myocardial ischemia produced by the occlusion; 2) cell activity increased at the onset of occlusion, adapted, and then increased again as ischemia developed (6 responses); 3) cell activity increased at the onset or release of occlusion, and rapidly adapted (13 responses) or remained elevated throughout the occlusion (2 responses); and 4) no response to occlusion (14 tests). Among the types of responses to occlusion, both the magnitude of increased cell activity as well as the spontaneous discharge rates were similar. There were no differences in types of response according to coronary artery ligated. Fourteen cells were tested for responses to separate occlusions of the LAD and CX. Ten cells responded differently to the two occlusions, and four cells exhibited similar responses. C-fiber input onto a neuron was significantly related to whether a cell exhibited a response to cardiac ischemia. Since every cell with C-fiber input did not respond to ischemia, however, this input was not sufficient to predict whether a cell would respond to ischemia. All cells had somatic fields, and all cells responded to noxious stimulation of the somatic field. Some cells also received input from hair movement. The modality of the effective somatic stimulus was not related to type of response to coronary artery occlusion. Spinothalamic and spinoreticular neurons responded similarly to occlusion. Type of response was neither related to cell location in spinal cord nor to projection site in brain. We conclude that spinothalamic and spinoreticular neurons respond to coronary artery occlusion. Different neurons may receive input from different regions of the heart as well as from different types of visceral afferents, resulting in various responses to occlusion. The population of cells excited from ischemia of a given portion of myocardium may determine how the brain interprets the noxious information and refers pain to different somatic structures.

Afferent Pathways↗
PubMed1983

Inhibition and excitation of thoracic spinoreticular neurons by electrical stimulation of vagal afferent nerves.

Neurons in spinal segments T1-T3 of cats projecting to the region of the nucleus reticularis gigantocellularis were tested for their responses to electrical stimulation of the vagus nerve. The effects of vagal efferent activity were blocked with methylatropine, thereby limiting vagal input to the effects of afferent fibers. Seventeen spinoreticular (SR) neurons were inhibited by vagal stimulation; one was excited; four were both inhibited and excited, and nine were unaffected. Half of the SR neurons were not spontaneously active; they were excited by somatic stimuli for 20- to 30-s periods in order to test for vagal inhibition. Vagal stimuli sometimes were sufficiently potent to completely suppress neuronal discharge during and just after 10-s periods of stimulation. Parameters of stimulus duration and frequency suggest activation of both A delta and C fibers in the vagus nerves. Vagal stimulation could inhibit increased firing from cardiac stimuli, such as coronary artery occlusion and injection of bradykinin into the heart. Two-thirds of the SR neurons so tested responded to bilateral sympathetic stimuli, whereas about one-half had excitatory somatic receptive fields restricted to the left foreleg and upper left side. The other half had bilateral, widespread, and complex somatic fields, including inhibitory responses. Such multiple inputs suggest an integrative role for spinoreticular neurons in sensory processing. Vagal inhibition and excitation of SR neurons probably operates via well known descending inhibitory systems from the nucleus raphe magnus and other medullary centers. The vagi are the only peripheral afferent pathway into this descending system that has been described to date.

Afferent Pathways↗
PubMed1983

Vagal afferent inhibition of primate thoracic spinothalamic neurons.

Spinothalamic (ST) neurons in the C8-T5 segments of the spinal cord were examined for responses to electrical stimulation of the left thoracic vagus nerve (LTV). Seventy-one ST neurons were studied in 39 anesthetized monkeys (Macaca fascicularis). Each neuron could be excited by manipulation of its somatic field and by electrical stimulation of cardiopulmonary sympathetic afferent fibers. LTV stimulation resulted in inhibition of the background activity of 43 (61%) ST neurons. Nine (13%) were excited, 3 (4%) were excited and then inhibited, while 16 (22%) did not respond. There was little difference among these groups in terms of the type of somatic or sympathetic afferent input although inhibited cells tended to be more prevalent in the more superficial laminae. The degree of inhibition resulting from LTV stimulation was related, in a linear fashion, to the magnitude of cell activity before stimulation. LTV inhibition of background activity was similar among wide dynamic range, high threshold, and high-threshold cells with inhibitory hair input. Any apparent differences in LTV inhibitory effects among these groups were accounted for by the differences in ongoing cell activity as predicted by linear regression analysis. LTV stimulation inhibited responses of 32 of 32 ST cells to somatic stimuli. In most cases the stimulus was a noxious pinch; however, LTV stimulation also inhibited responses to innocuous stimuli such as hair movement. Bilateral cervical vagotomy abolished the inhibitory effect of LTV stimulation on background activity (six cells) or responses to somatic stimuli (seven cells). Stimulation of the cardiac branch of the vagus inhibited activity of three cells to a similar degree as LTV stimulation, while stimulation of the vagus below the heart was ineffective in reducing activity of 10 cells. We conclude that LTV stimulation alters activity of ST neurons in the upper thoracic spinal cord. Vagal inhibition of ST cell activity was due to stimulation of cardiopulmonary vagal afferent fibers coursing to the brain stem, which appear to activate descending inhibitory spinal pathways. Vagal afferent activity may participate in processing of somatosensory information as well as information related to cardiac pain.

Afferent Pathways↗
PubMed1983

Vagal afferent inhibition of spinothalamic cell responses to sympathetic afferents and bradykinin in the monkey.

Effects of stimulating the left thoracic vagus nerve on the responses of spinothalamic neurons to electrical stimulation of cardiopulmonary sympathetic afferent fibers and to intracardiac injections of bradykinin were determined. Experiments were performed on 39 monkeys (Macaca fascicularis) tranquilized with ketamine and anesthetized with alpha-chloralose. The 30 spinothalamic cells studied had the following characteristics. They were excited by manipulation of their somatic receptive fields, were excited by electrical stimulation of cardiopulmonary sympathetic afferent fibers, and exhibited viscerosomatic convergence. Responses of 15 of 19 cells to sympathetic afferent test stimuli were inhibited by conditioning stimuli applied to left thoracic vagus nerve. A conditioning-test interval of 40-50 msec resulted in maximal inhibition of responses to both A delta and C fiber sympathetic afferents. A long time course of inhibition was present to at least a conditioning-test interval of 200 msec. Left thoracic vagus nerve stimulation inhibited 14 of 14 cells responding to intracardiac injection of bradykinin. Entrainment of activity of five cells to the cardiac cycle occurred in response to bradykinin. In each case, left thoracic vagus nerve stimulation, in addition to reducing frequency of cell discharge, disrupted the cardiac related pattern of cell activity. Bilateral cervical vagotomy abolished all inhibitory effects of left thoracic vagus nerve stimulation. These results demonstrate that vagal afferents may participate in processing of information related to cardiac pain.

Angina Pectoris↗
PubMed1982

Responses of primate spinothalamic neurons located in the sacral intermediomedial gray (Stilling's nucleus) to proprioceptive input from the tail.

Extracellular an intracellular recordings were obtained from 24 spinothalamic neurons located in the intermediomedial gray (Stilling's nucleus) in the S2 and S3 spinal segments of anesthetized adult monkeys (Macaca fascicularis). Most units were spontaneously active. They lacked cutaneous receptive fields but could be excited by subcutaneous receptors. Bending the tail to one side of the animal's body axis excited cells located on the contralateral side of the cord an inhibited ipsilateral cells. The firing rate of each cell was a reproducible function of the angle of the portion of the tail distal to the innervated segment. Cells responded with a burst of spikes to electrical stimulation of low threshold ipsilateral primary afferent fibers in the homosegmental dorsal root. The latency of the underlying synaptic potential was 0.5-0.7 ms from the time of arrival of the afferent volley at the cord, indicating monosynaptic input. Low intensity stimulation of the contralateral homosegmental dorsal root inhibited back-ground activity. The latency of the underlying inhibitory synaptic potential was 0.8-1.1 ms, suggesting crossed disynaptic inhibition. We conclude that sacral spinothalamic tract neurons located in the intermediomedial gray participate in signalling the spatial orientation of the animal's tail.

Animals↗