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Biomedical subjects

R D Foreman

Publications and source records attributed to R D Foreman.

At least 73 records · Page 4Linked to original sources
PubMed1990

Urinary bladder and hindlimb stimuli inhibit T1-T6 spinal and spinoreticular cells.

Upper thoracic spinal neurons are primarily excited by cardiopulmonary spinal afferent input but are excited and inhibited by splanchnic afferent input. These data suggest that the greater the number of segments between a spinal neuron and spinal afferent input the greater the probability that the afferent input will inhibit the spinal neuron. Based on this idea we hypothesized that visceral (urinary bladder) and somatic (hindlimb) afferent input would inhibit upper thoracic spinal neurons. To test this hypothesis the activities of 69 spinal and 27 spinoreticular tract neurons in 45 alpha-chloralose-anesthetized cats were studied. Only neurons excited by both visceral and somatic thoracic afferent input were studied. Urinary bladder distension (UBD) inhibited 48 (50%), excited 6 (6%), and did not affect 41 (43%) of these neurons. Also, UBD inhibited the excitatory responses of these cells to noxious visceral and somatic stimuli. Hindlimb pinch also inhibited greater than 50% of the neurons. These data indicate that visceral and somatic afferent input to the lumbosacral spinal cord inhibits the activity of upper thoracic neurons. This inhibitory effect may play a role in localization of sensory and motor responses to noxious stimuli.

Afferent Pathways↗
PubMed1989

Effects of chemical and electrical stimulation of the midbrain on feline T2-T6 spinoreticular and spinal cell activity evoked by cardiopulmonary afferent input.

Responses to electrical and chemical stimulation of the periaqueductal gray (PAG) and midbrain reticular formation (RF) were examined on extracellular activity of 28 spinoreticular tract (SRT) and 56 spinal neurons in T2-T6 segments of anesthetized cats. All cells received excitatory viscerosomatic convergent input from the left forelimb triceps region and from cardiopulmonary sympathetic afferents. Evoked activity that resulted from pinching the left triceps was reduced by PAG and midbrain RF stimulation (100 Hz, 100 microseconds, 50-500 microA). Visceral afferent input to the neurons was elicited during electrical stimulation of cardiopulmonary sympathetic afferent fibers and following injection of bradykinin into the left atrium of the heart. Electrical stimulation of the PAG and adjacent RF decreased A-delta and C-fiber activation of these neurons produced during electrical stimulation of cardiopulmonary afferents and decreased the activity of cells during excitatory responses to intracardiac bradykinin. Electrical stimulation of the PAG or midbrain RF similarly decreased spontaneous and evoked cell activity. Selective activation of cell bodies with microinjection of glutamate into the PAG reduced the activity of 6 of 8 cells whereas glutamate injections into midbrain RF reduced the activity of only 3 of 13 neurons. This difference in the effectiveness of chemically stimulating the PAG vs midbrain RF was significant (P less than 0.05). These data demonstrate that (1) neuronal activity evoked by visceral afferent input from the heart was decreased by electrical stimulation of the PAG and midbrain RF and (2) a portion of this descending inhibition may be mediated by cell bodies in the PAG.

Action Potentials↗
PubMed1989

Ventrolateral medullary lesions and fastigial cardiovascular response in beagles.

These studies were designed to verify that the putative vasomotor center in the rostral ventrolateral medulla (RVLM) contained the outflow paths for the fastigial nucleus (FN) sympathoexcitatory cardiovascular response. If so, then lesions placed by radiofrequency heating (75 degrees C) or application of kainic acid (40 mM) pledgets would reduce or ablate the pressor-tachycardia response after electrical stimulation of FN. Anesthetized beagles (alpha-chloralose, 115 mg/kg) were used in this study to maintain consistency in medullary brain stem anatomy. A ventral brain stem approach exposed the three chemosensitive zones of Mitchell, Schlaefke, and Loeschcke. In other species the intermediate zone and a portion of the rostral zone underlie the Hokfelt C1 cell group and the putative RVLM vasomotor center. Heart rate, arterial and left ventricular (LV) pressures, and maximal rate of pressure development (LV dp/dt) increased 14-84% above control levels in response to stimulating FN 5-10 times the stimulation threshold. The cardiovascular response was abolished in four of six dogs that received bilateral radiofrequency lesions at a depth of 1-2 mm. In five of seven dogs that received kainate surface lesions, the response was substantially reduced but not abolished. These lesions were effective only in the RVLM, above the corresponding intermediate, but not adjacent rostral or caudal chemosensitive areas. The data support the hypotheses of others that an epinphrine-containing cell group in this region is a final common pathway of sympathoexcitation. Expression of the FN cardiovascular response is primarily mediated through this vasomotor region previously identified by others in the rat, cat, rabbit, and primate.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Effects of intracardiac bradykinin and capsaicin on spinal and spinoreticular neurons.

The responses of thoracic spinal and spinoreticular tract (SRT) neurons to activation of cardiac spinal afferents by injections of bradykinin (BK) and capsaicin (CAP) into the left atrium or pericardial sac were determined in vagotomized cats anesthetized with alpha-chloralose. Activities of spinal and SRT neurons in the T1-T5 spinal cord were recorded extracellularly. All neurons received excitatory somatic and cardiopulmonary sympathetic afferent input. Application of BK and CAP to the heart excited most SRT neurons and many spinal neurons but also inhibited some spinal neurons. The two drugs often affected spinal but not SRT neurons differently. Capsaicin excited high threshold and high threshold inhibitory neurons but not wide-dynamic range spinal neurons. In contrast, BK excited all three categories of spinal and SRT neurons. The differential responses of spinal neurons to intracardiac BK and CAP suggested that these compounds can stimulate functionally different populations of cardiac sympathetic afferents.

Animals↗
PubMed1989

Cardiac and abdominal vagal afferent inhibition of primate T9-S1 spinothalamic cells.

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.

Abdomen↗
PubMed1989

Urinary bladder and hindlimb afferent input inhibits activity of primate T2-T5 spinothalamic tract neurons.

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.

Action Potentials↗
PubMed1988

Activation of feline spinal neurones by potentiated ventricular contractions and other mechanical cardiac stimuli.

1. Neurones in the spinal cord were tested for responses to premature ventricular contractions (PVCs), produced by controlled electrical extra stimuli, and other mechanical stimuli applied to the heart. Thirty-eight neurones were antidromically activated from the medial medullary reticular formation and/or the caudal thalamus, and twenty-four neurones did not project to these sites. 2. Only those neurones excited by electrical stimulation of the left stellate ganglion were tested for responses to PVCs. A total of twenty neurones (32%) responded to electrically induced PVCs. Three major patterns of responses occurred. Three neurones exhibited an early burst and a late burst (or bursts) during the arrhythmia, one neurone fired only an early burst, and sixteen neurones responded with only a late burst. The early bursts occurred shortly after the onset of the compensatory pause accompanying the PVC; the late bursts were usually associated with the subsequent potentiated contraction, although the stimulus eliciting the burst must often have occurred late in the compensatory pause. 3. Responses to PVCs were only seen in neurones receiving C fibre and A delta fibre input. However, there were some neurones with both A delta and C input that did not respond to PVCs. No neurones with only A delta input responded to PVCs. 4. Neurones projecting to thalamus were less likely to respond to PVCs than either spinoreticular neurones or neurones with unidentified projections. 5. Neurones responsive to PVCs were likely to exhibit a cardiac rhythmicity in their spontaneous or evoked activity. 6. A total of 42% of tested neurones responded to a rapid infusion of saline into the heart, 52% had a cardiac receptive field, and 74% responded to aortic occlusion. A given neurone might respond to one or more of these stimuli, without responding to every mechanical stimulus tested. 7. Cervical vagotomy never abolished a response to PVCs, although either the spontaneous discharge rate or magnitude of response was sometimes altered. 8. Neurones responsive to PVCs were also responsive to intracardiac bradykinin. In addition, 95% of the neurones received convergent somatic input. 9. We conclude that about a third of spinal neurones excited by electrical stimulation of the left stellate ganglion receive information regarding mechanical, presumably innocuous, events in the heart. Most responsive neurones also receive somatic input and noxious cardiac input, and this information is transmitted to the thalamus, reticular formation, and probably to other spinal segments.

Action Potentials↗
PubMed1988

Central organization of sympathetic cardiovascular response to pain.

Figure 1 summarizes the pathways discussed in this review. Noxious and innocuous cardiac and somatic information converge on SRT neurons in the upper thoracic spinal cord; the third thoracic segment (T3) is shown in Figure 1. The SRT pathway and collaterals of the STT convey this information to the MRF (mainly RGC). This input is integrated with other inputs (eg. auditory and visual) by MRF neurons, some of which project to the spinal cord. RS motor neurons (dotted pathway) might mediate motor responses to cardiac pain, as well as motor responses associated with escape or alerting behavior. RS neurons (cross-hatched and clear pathways) can also modulate ascending traffic by altering activity of SRT and STT cells. Finally, RS neurons (dotted pathway) might modify sympathetic function via collaterals to IML or to interneurons, or MRF cells could project to medullary areas possessing neurons (solid pathway) that project directly to IML. The small figurines represent the heart (top), blood vessels (middle right) and muscle (bottom).

Animals↗
PubMed1988

Autonomic mechanisms and sudden death. New insights from analysis of baroreceptor reflexes in conscious dogs with and without a myocardial infarction.

We have suggested that among conscious dogs with a healed anterior wall myocardial infarction (MI) a depressed baroreflex sensitivity (BRS) carries a higher risk of developing ventricular fibrillation during a brief ischemic episode associated with an exercise stress test. The clinical and pathophysiological implications of our previous findings prompted the present study, which addressed three major questions: 1) Is, indeed, analysis of BRS after MI a specific and sensitive marker for sudden death-risk stratification? 2) Does MI modify BRS? 3) Does analysis of BRS before MI provide information about outcome during ischemic episodes occurring after MI? An anterior MI was produced in 301 dogs, and 4 weeks later, a 2-minute circumflex coronary artery occlusion beginning during the last minute of an exercise stress test could be performed in 192 animals. Ventricular fibrillation occurred in 106 (55%) dogs (susceptible to sudden death), whereas 86 (45%) dogs (resistant to sudden death) survived. BRS was assessed by the phenylephrine method and was expressed by the regression line relating RR intervals to blood-pressure changes. BRS was significantly lower among susceptible than among resistant dogs (9.1 +/- 6.0 vs. 17.7 +/- 6.5 msec/mm Hg, p less than 0.0001). The risk for sudden death increased from 20% (15 of 73 dogs) for a BRS greater than 15 msec/mm Hg to 91% (62 of 68 dogs) for a BRS less than 9 msec/mm Hg (p less than 0.001). An internal control study in 55 animals showed that BRS was reduced 4 weeks after MI compared with control conditions (13.5 +/- 6.7 vs. 17.8 +/- 6.6 msec/mm Hg, p less than 0.001) and that a reduction occurred in 73% of animals. Susceptible dogs and those that spontaneously died after MI had a lower BRS even before the MI (16.2 +/- 5.9 vs. 22.2 +/- 6.2 msec/mm Hg, p less than 0.001). The risk for sudden death after MI increased from 35% (nine of 26 dogs) for a BRS before MI greater than 20 msec/mm Hg to 85% (17 of 20 dogs) for a BRS before MI less than 14 msec/mm Hg (p less than 0.001). This study demonstrates that the presence of a reduced BRS is associated with a greater susceptibility to ventricular fibrillation during subsequent ischemic episodes. In the majority of dogs, BRS is reduced after an MI. The results in 192 conscious dogs with a healed MI indicate that analysis of BRS is a powerful tool for risk stratification not only after, but even before, the occurrence of an MI.

Animals↗
PubMed1987

Effects of stimulating the subcoeruleus-parabrachial region on the non-noxious and noxious responses of T1-T5 spinothalamic tract neurons in the primate.

The effects of electrical stimulation of the subcoeruleus-parabrachial (SC-PB) region on the discharge rate of upper thoracic spinothalamic tract (STT) neurons were investigated in 21 monkeys anesthetized with alpha-chloralose. STT cells were antidromically activated from the medial thalamus (MT) and the ventral posterior lateral nucleus (VPL) and received viscerosomatic convergent input from the cardiopulmonary sympathetic afferents and the left chest-forearm region. Stimulation of the SC-PB region inhibited the activity of all 30 STT neurons studied in the T1-T5 regions of the spinal cord. The minimum average current required to decrease the discharge rate of 22 cells exhibiting spontaneous activity was 89 +/- 10 microA (100 Hz, 100 microseconds duration). Currents as high as 300 microA completely inhibited the activity of most cells. Examination of the importance of frequency of stimulation from the SC-PB area on 8 cells revealed that impulses of at least 40 Hz (208 +/- 37 microA, 100 microseconds duration) were necessary to inhibit the spontaneous activity by 60%. Higher frequencies produced greater degrees of inhibition. Stimulation of the SC-PB region also inhibited the response of 23 of 23 neurons excited by noxious pinch and 11 of 11 wide dynamic range cells stimulated by innocuous input such as blowing or brushing hair. No differences in the inhibition produced by SC-PB stimulation on cells projecting to VPL (n = 20), MT (n = 5), or both VPL and MT (n = 5) were observed. These results demonstrate that the SC-PB region may be an important brainstem site for descending inhibition of both noxious and innocuous somatic input to upper thoracic STT cells in the primate.

Animals↗
PubMed1987

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.

Action Potentials↗
PubMed1986

Fastigial nucleus modulation of medullary parasolitary neurons.

Input from the cerebellar fastigial nuclei to neurons at the lateral margin of the nuclei of the solitary tract, particularly to the area identified as the nucleus parasolitarius was investigated in acutely prepared, anesthetized dogs. Fastigial nucleus stimulation led to short latency excitation of nucleus parasolitarius units often followed by prolonged inhibition of spontaneous activity. Excitation from deep skeletal muscle afferents, converged on 25% of the spontaneously active units excited from the fastigial nuclei; these afferents originated primarily from the ipsilateral forelimb muscles. This study provides electrophysiological evidence for fastigial modulation of neurons previously demonstrated autoradiographically to receive presumed monosynaptic fastigial nucleus efferents. The convergence of forelimb muscle afferent information tentatively identified as being from Group Ia or Group II pressure stretch receptors suggests that the nucleus parasolitarius may be an integrative area for cerebellar, sensorimotor and/or autonomic information.

Animals↗
PubMed1986

Fastigial nucleus projections in the midbrain and thalamus in dogs.

Efferent connections to midbrain and thalamus from portions of the cerebellar fastigial nucleus were investigated using autoradiographic techniques. Bipolar stimulating electrodes were placed in the fastigial nucleus of anesthetized beagles and the area which produced maximal increases in blood pressure and heart rate was localized in each dog. A mixture of [3H]leucine and [3H]proline (4:1) was injected into that area and autoradiograms were prepared. Injections filled the rostral and various parts of the caudal fastigial nucleus. The rostral-caudal extent of injection sites were mapped in the horizontal plane from sequential coronal, thionin-stained sections and "primary" and "secondary" injection zones were defined according to specific criteria. Labeled axons reached the mesencephalon via the contralateral uncinate fasiculus. Ascending fibers assembled in a diffuse contingent at the prerubral level adjacent to the ventrolateral periaqueductal gray. The heaviest projections were contralateral to the injection site, but ipsilateral terminals were observed as well. In the midbrain, axons entered the contralateral and ipsilateral superior colliculus to branch repeatedly and terminate in the deep and intermediate layers. Additional terminals were observed bilaterally in the nuclei of the posterior commissure and pretectal areas at the midbrain-diencephalic junction. In the thalamus, labeled axons formed into three groups which terminated in: the contralateral paraventricular complex and medial dorsal nucleus; the contralateral central medial, paracentral, parafasicular and central lateral nuclei, and the contralateral ventral medial and ventral lateral nuclei. There was a sparse projection to the ipsilateral ventral lateral nucleus. The contralateral projection to the ventral medial and ventral lateral nuclei was marked by dense clusters of label ventral to the internal medullary lamina extending, in the dorsal ventral lateral nucleus, to its rostral pole. Projections to specific somesthetic thalamus or the hypothalamus were not observed. These ascending projections in the canine brain generally conform to those described in other nonprimate mammals. The fastigial nucleus presumably provides information concerning equilibrium and body proprioception to the superior colliculus and to thalamic nuclei including both specific motor relay and "nonspecific" midline and intralaminar nuclei, much the same as reported in the cat. The projection to the ventral medial and ventral lateral thalamic nuclei terminate in areas known to participate in the control of axial and proximal limb muscle activity.(ABSTRACT TRUNCATED AT 400 WORDS)

Amino Acids↗
PubMed1986

Fastigial nucleus cardiovascular response and brain stem lesions in the beagle.

Changes in the excitatory cardiovascular response (heart rate, arterial blood pressure, left ventricular pressure, and LV dP/dt as an index of myocardial contractility) resulting from electrical stimulation of the cerebellar fastigial nucleus (FN) were recorded after placement of DC or radio-frequency lesions or after microinjections of kainic acid into brain stem areas that receive FN projections and have been shown to be involved in central cardiovascular control. FN-induced increases in heart rate, blood pressure, and contractility were reduced or abolished by lesions made in the restiform body or the A5 area, which is homologous to the catecholamine-containing region in cats and rats. Lesions in the paramedian reticular nucleus, rostral and caudal to obex, failed to reduce the FN cardiovascular response. Nucleus of the solitary tract lesions augmented the FN pressor response and tachycardia. Kainic acid (1 microliter of 100 mM solution) caused profound depression of heart rate, blood pressure, and contractility and reduced or eliminated the FN-induced cardiovascular response when injected into the A5 area, previously identified by the pressor response following electrical stimulation. We concluded from these observations that a descending fastigiobulbar sympathoexcitatory pathway courses through a previously identified A5 pressor area that is also capable of a depressor response when the cell bodies alone are activated.

Animals↗
PubMed1986

Periventricular gray inhibition of thoracic spinothalamic cells projecting to medial and lateral thalamus.

Effects of electrical stimulation of the periventricular gray (PVG) on spinothalamic tract (STT) cell activity were determined in 19 anesthetized monkeys (Macaca fascicularis). Twenty-two STT cells projected to the ventral posterior lateral nucleus (L-STT cells), 11 to the medial thalamus (M-STT cells), and 9 to both thalamic regions (LM-STT cells). All cells had somatic receptive fields and responded to electrical stimulation of cardiopulmonary sympathetic afferent fibers. PVG stimulation inhibited activity of 41 of 42 STT cells. Degree of inhibition of background activity was related to intensity and frequency. Stimulus currents of 300 microA or less completely silenced background activity of most cells. Thresholds for stimulus current averaged 100 +/- 20 microA and were unrelated to cell projection site, laminar location, or type of somatic or visceral input. However, lowest thresholds were found when the PVG electrodes were located within 0.5 mm of the third ventricle in the dorsomedial hypothalamus or nucleus reuniens of the thalamus. PVG stimulation inhibited responses of 22 of 22 cells to intracardiac injections of bradykinin. Bradykinin (2 micrograms/kg) increased cell activity from 15 +/- 3 to 31 +/- 5 spikes/s (P less than 0.01), and PVG stimulation (380 +/- 40 microA) reduced activity to 9 +/- 3 spikes/s (P less than 0.001). PVG stimulation inhibited responses of 33 of 33 STT cells to noxious pinch of skin or skin and muscle and responses of 8 of 8 cells to hair movement. Degree of inhibition of cell responses to noxious pinch was not significantly different from inhibition of responses to bradykinin. Effects of PVG stimulation on activity of six STT cells were studied before and after bilateral lesions were made in the dorsolateral funiculus (DLF). In no case did the lesions abolish or attenuate inhibitory effects of PVG stimulation. These results suggest that PVG may participate in descending inhibition of STT cells including cells mediating cardiac pain. The descending pathways are not located in the DLF. Further, descending inhibitory systems modulate STT cells projecting to both medial and lateral thalamus.

Afferent Pathways↗