Esophagocardiac convergence onto thoracic spinal neurons: comparison of cervical and thoracic esophagus

The aim of this study was to characterize thoracic spinal neurons receiving convergent inputs from the esophagus, heart and somatic receptive fields. Extracellular potentials of single T3-T4 spinal neurons were recorded in pentobarbital anesthetized male rats. Thoracic and cervical esophageal distensions (TED, CED) were produced by water inflation of a latex balloon. A catheter was placed in the pericardial sac to administer bradykinin or a mixture of algogenic chemicals. 96/311 (31%) neurons responded to both TED and intrapericardial chemicals (IC) and 48/177 (27%) neurons responded to both CED and IC. Long-lasting excitatory responses were more frequently encountered (P<0.05) in esophagocardiac spinal neurons responding to TED (T-ECSNs, 62/91) than in neurons responding to CED (C-ECSNs, 23/47). Ninety-one percent of T-ECSNs and 98% of C-ECSNs had somatic fields on chest, axilla and upper back areas. Esophagocardiac convergence on thoracic spinal neurons provided a spinal mechanism that might mediate viscerovisceral nociception and reflexes.     

Differential effects of urinary bladder distension on high cervical projection neurons in primates

Projection neurons located in high cervical segments of primates are generally excited instead of inhibited by cardiopulmonary spinal inputs, which enter thoracic dorsal roots. Thus, high cervical neurons with axons that either ascend to the thalamus or descend to thoracolumbar spinal segments can process and transmit excitatory cardiac information. The purpose of this study was to determine whether the excitatory effects observed to cardiopulmonary afferent stimulation are a universal response in high cervical projection neurons to spinal visceral inputs. Urinary bladder distension (UBD) was used to stimulate visceral afferent inputs that enter lumbosacral dorsal roots. Effects were determined on extracellular activity of either spinothalamic tract (STT) neurons or descending propriospinal neurons that were recorded in high cervical segments of anesthetized monkeys. Results showed that 17/34 STT neurons were inhibited by UBD and 3/34 STT neurons were excited. Widespread visceral inputs, therefore, can excite high cervical STT neurons but the majority of responsive STT neurons were inhibited by UBD. Effects of UBD on high cervical descending propriospinal neurons were significantly different from responses in STT neurons. Extracellular activity of fewer propriospinal neurons was affected by UBD and responses were more variable; 3/26 neurons were inhibited, 5/26 neurons were excited and one neuron was excited/inhibited by UBD. These results showed that the generally excitatory responses of high cervical projection neurons to cardiopulmonary inputs were not duplicated by stimulation of sensory input from the urinary bladder. Furthermore, results of this study indicated that effects of sensory inputs on spinal neurons might vary depending on axonal projections of the neurons examined.     

Convergence of trigeminal input with visceral and phrenic inputs on primate C1-C2 spinothalamic tract neurons.

Trigeminal, spinal and vagal afferent fibers overlap in C1-C2 segments. We hypothesized that trigeminal input from the superior sagittal sinus (SSS) can excite C1-C2 spinothalamic tract (STT) neurons receiving thoracic visceral or phrenic inputs. Effects of SSS stimulation were evenly divided among cells responding to each nerve stimulus; magnitude of responses to ipsilateral vagal input was greater in neurons excited by SSS input. Somatic fields of 80% of neurons responding to SSS stimulation included face areas innervated by the trigeminal nerve, whereas somatic fields of 89% of neurons unaffected by SSS stimulation were located only on areas innervated by cervical spinal nerves. Results are consistent with the idea that pain referred to trigeminal areas could originate in thoracic organs.     

Convergence of trigeminal input with visceral and phrenic inputs on primate C1–C2 spinothalamic tract neurons

Trigeminal, spinal and vagal afferent fibers overlap in C1–C2 segments. We hypothesized that trigeminal input from the superior sagittal sinus (SSS) can excite C1–C2 spinothalamic tract (STT) neurons receiving thoracic visceral or phrenic inputs. Effects of SSS stimulation were evenly divided among cells responding to each nerve stimulus; magnitude of responses to ipsilateral vagal input was greater in neurons excited by SSS input. Somatic fields of 80% of neurons responding to SSS stimulation included face areas innervated by the trigeminal nerve, whereas somatic fields of 89% of neurons unaffected by SSS stimulation were located only on areas innervated by cervical spinal nerves. Results are consistent with the idea that pain referred to trigeminal areas could originate in thoracic organs.     

Afferent pathway and neuromodulation of superficial and deeper thoracic spinal neurons receiving noxious pulmonary inputs in rats

The occurrence of vagally mediated afferent signaling by lung irritants is well known. However, spinal visceral afferent pathways also might be relevant to pulmonary irritation. In the present study, responses and modulation of superficial and deep T3 spinal neurons were examined using inhaled ammonia, and the peripheral afferent fibers were also characterized in part. Extracellular potentials of single thoracic (T3) spinal neurons were recorded in pentobarbital anesthetized, paralyzed, and ventilated male rats. Ammonia vapor (0.5, 1.0, 2.0 ml) was injected into the inspiratory line of the ventilator for 20 s. Inhaled ammonia (IA, 1.0 ml) excited 5/6 neurons and inhibited one spinal neuron recorded in superficial laminae, whereas deeper neurons responded with excitatory (E, n = 20), inhibitory (I, n = 4) or biphasic patterns (6 E-I, 3 I-E). Electrical and chemical stimulation of C1-C2 spinal neurons primarily suppressed T3 neuronal responses to IA. Resiniferatoxin (2 microg/kg, i.v.), which desensitizes afferent fibers containing transient receptor potential vanilloid receptor-1 (TRPV-1), abolished excitatory responses of 8/8 neurons to IA. Bilateral cervical vagotomy did not affect IA responses in 5 superficial neurons while 7 deeper neurons showed variable responses. 82% (32/39) of the spinal neurons responding to IA also received convergent noxious inputs from somatic fields in the chest and back areas. These results suggested that superficial and deeper spinal neuronal activation by inhaled ammonia mainly depended upon pulmonary sympathetic afferent fibers expressing TRPV-1. Additionally, C1-C2 spinal neurons, supraspinal sites and vagal afferents modulated the thoracic spinal neuronal responses to lower airway irritation.     

Effects of urinary bladder distension on activity of T3-T4 spinal neurons receiving cardiac and somatic noxious inputs in rats

The aims of this study were to examine effects of urinary bladder distension (UBD) on T(3)-T(4) spinal neurons receiving cardiac and somatic noxious inputs and to determine the pathway involved in transmitting urinary bladder inputs to thoracic spinal segments. Extracellular potentials of single T(3)-T(4) neurons were recorded in pentobarbital anesthetized male rats. Either bradykinin solution (10(-5) M) or an allogenic mixture (adenosine 10(-3) M, bradykinin, histamine, serotonin, prostaglandin E2 10(-5) M each) was administered intrapericardially. UBD was produced by saline inflation (0.5-2.0 ml, 20 s). Of 487 neurons tested for responses to UBD, 70 were inhibited and 37 were excited. Seventy-six out of 336 neurons received convergent input from UBD and heart; 69/76 viscerovisceral convergent neurons had somatic fields. Spinal transection at rostral C(1) abolished UBD inhibition in 5/9 neurons; whereas transections at L(1)-L(2) abolished UBD inhibition in 3/3 cells tested. Results showed that T(3)-T(4) spinal neurons processing cardiac and somatic nociceptive information were primarily inhibited by input from the urinary bladder through either supraspinal structures or direct intraspinal pathways.     

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.     

Responses and afferent pathways of C(1)-C(2) spinal neurons to gastric distension in rats

Some evidence shows that the upper cervical spinal cord might play an important role in propriospinal processing as a sensory filter and modulator for visceral afferents. The aims of this study were to determine (1). the responses of C(1)-C(2) spinal neurons to gastric distension and (2). the relative contribution of vagal and spinal visceral afferent pathways for transmission of gastric input to the upper cervical spinal cord. Extracellular potentials of single C(1)-C(2) spinal neurons were recorded in pentobarbital anesthetized male rats. Graded gastric distension (20-80 mm Hg) was produced by air inflation of a latex balloon surgically placed in the stomach. Sixteen percent of the neurons (32/198) responded to gastric distension; 17 neurons were excited and 15 neurons were inhibited by gastric distension. Spontaneous activity of neurons with inhibitory responses was higher than those neurons with excitatory responses (18.1+/-2.7 vs. 3.8+/-1.7 impulses s(-1), p<0.001). Twenty-eight of thirty-two (87.5%) neurons responded to mechanical stimulation of somatic fields on head, neck, ears or shoulder. Most lesion sites of neurons with excitatory responses were found in laminae V, VII; however, neurons with inhibitory responses were in laminae III, IV. Bilateral cervical vagotomy abolished responses of 4/8 neurons tested. Spinal transection at C(6)-C(7) abolished responses of the other four neurons that still responded to gastric distension after bilateral vagotomy. Results of these data supported the concept that a group of C(1)-C(2) spinal neurons might play a role in processing sensory information from the stomach that travels in vagal and spinal visceral afferent fibers.     

Somatic afferent modulation of thoracic (T9‐T10) spinal neurons receiving gastric mechanical input in rats

Objectives: The aim was to determine whether somatic afferent fiber stimulation influences thoracic spinal neuronal activity responding to gastric distensions. Materials and Methods: Extracellular potentials of single T9‐T10 spinal neurons were recorded in anesthetized male rats. Ipsilateral median and peroneal nerve afferent stimulation (MNAS, PNAS) was delivered by electrodes. Inflation of a latex balloon was used to produce gastric distension. Results: MNAS and PNAS (1.5 mA, 50 Hz, 10 sec) altered activity of 63% and 66% of the spinal neurons excited or inhibited by gastric distension, respectively. MNAS more frequently reduced spinal neuronal activity with excitatory responses to gastric distension than did PNAS (p < 0.05). PNAS more likely increased neuronal activity with low‐threshold excitatory responses to gastric distension than MNAS (p < 0.05). Conclusions: Peripheral somatic afferent information utilizes central pathways to modulate gastric afferent processing in T9‐T10 spinal neurons. Thus, somatic afferent stimulation might be used to treat gastric pain and/or hypersensitivity.     

Chemical activation of cardiac receptors affects activity of superficial and deeper T3-T4 spinal neurons in rats

The purposes of this study were to examine responses of superficial (depth <300 microm) and deeper thoracic spinal neurons to chemical stimulation of cardiac afferents and effects of descending influences on these neurons. Extracellular potentials of single T(3)-T(4) neurons were recorded in pentobarbital anesthetized, paralyzed and ventilated male rats. A catheter was placed in the pericardial sac to administer 0.2 ml of a mixture of algogenic chemicals that contained adenosine (10(-3) M), bradykinin, histamine, serotonin, prostaglandin E(2) (10(-5) M). Fifteen of 55 (27%) superficial neurons responsive to intrapericardial chemicals were compared to 80/169 (47%) deeper neurons. All 15 superficial neurons that responded to cardiac afferents were excited (E), whereas 66 deeper neurons were excited, ten were inhibited and four showed excitation-inhibition. Spontaneous activity of superficial neurons with short-lasting excitatory responses was significantly lower than that of deeper neurons (P<0.05). Somatic receptive fields on chest, axilla, arm and upper back areas were found for 77/95 (81%) neurons that responded to intrapericardial chemicals. The proportion of somatic field properties and their sizes in superficial neurons were similar to deeper neurons. After cervical spinal transection, both spontaneous activity and responses to chemical stimulation of cardiac afferents significantly increased in six out of six neurons excited by intrapericardial injections. Results showed that chemical stimulation of cardiac afferents excited superficial T(3)-T(4) spinal neurons, whereas deeper neurons exhibited multiple patterns of responses. Some characteristics of subgroups of superficial neurons were quantitatively different from deeper neurons. Thoracic spinal neurons processing cardiac nociceptive information were under tonic descending inhibition.     

Responses of cat C1 spinal cord dorsal and ventral horn neurons to noxious and non-noxious stimulation of the head and face

Previous anatomical studies have shown that trigeminal and cervical afferent nerve fibers project to the upper cervical segments of the spinal cord. To determine the response properties of neurons in the upper cervical spinal cord, we studied the response of C1 dorsal and ventral horn cells to electrical and graded mechanical stimulation of the face, head and neck in anesthetized cats. Neurons were classified as low-threshold-mechanoreceptive (LTM), wide-dynamic-range (WDR), nociceptive-specific (NS) or unresponsive, based on their responsiveness to graded mechanical stimulation. Extracellular single unit recordings were obtained from 118 neurons excited by cervical (24), trigeminal (39) or both cervical and trigeminal (55) stimulation and from 24 neurons unresponsive to peripheral stimulation. Based on neuronal mechanical response properties, 52.2% of the responsive neurons were classified as LTM, 35.9% as WDR and 11.9% as NS. WDR neurons exhibited more convergence and had larger receptive fields than either NS or LTM neurons. WDR and NS neurons had longer first spike latencies than LTM neurons at all tested sites. Only WDR neurons were found to project to the contralateral caudal thalamus. Within C1, LTM neurons were located primarily in laminae III and IV, WDR neurons in lamina V and NS neurons in laminae VII and VIII. These data suggest that some neurons in the first cervical segment of the spinal cord receive convergent input from trigeminal and cervical pathways and may be involved in mediating orofacial and cranial pain.     

Spinal segmental sympathetic outflow to cervical sympathetic trunk, vertebral nerve, inferior cardiac nerve and sympathetic fibres in the thoracic vagus

The spinal segmental localization of preganglionic neurons which convey activity to the sympathetic nerves, i.e. vertebral nerve, right inferior cardiac nerve, sympathetic fibres in the thoracic vagus and cervical sympathetic trunk, was determined on the right side in chloralose anaesthetized cats. For that purpose the upper thoracic white rami were electrically stimulated with a single pulse, suprathreshold for B and C fibres, and the evoked responses were recorded in the sympathetic nerves. The relative preganglionic input from each segment of the spinal cord to the four sympathetic nerves was determined from the size of the evoked responses. It was found that each sympathetic nerve receives a maximum preganglionic input from one segment of the spinal cord (dominant segment) and that the preganglionic input gradually decreased from neighbouring segments. The spinal segmental preganglionic outflow to the cervical sympathetic trunk, thoracic vagus, right inferior cardiac nerve and vertebral nerve gradually shifted from the most rostral to the most caudal spinal cord segments. In some cases, a marked postganglionic component was found in the cervical sympathetic trunk. It was evoked by preganglionic input from the same spinal cord segments which transmitted activity to the vertebral nerve. These results indicate that there is a fixed relation between the spinal segmental localization of preganglionic neurons and the branch of the stellate ganglion receiving the input from these neurons.     

Role of cervical neurons in propriospinal inhibition of thoracic dorsal horn neurons.

We previously reported that electrical or glutamate stimulation of the cervical spinal cord elicits a 40-60% decrease in renal sympathetic nerve activity (RSA) in the anesthetized rats. This sympatho-inhibition was possible, however, only after transection of the spinal cord at C1 or GABAergic inhibition of neurons in the rostral ventrolateral medulla. We postulated that cervical neurons inhibit RSA by inhibiting the activity of spinal interneurons that are antecedent to sympathetic preganglionic neurons (SPNs), and that these interneurons may be, in turn, excited by afferent signals. In this study, we tested the hypothesis that cervical neurons can inhibit visceroceptive thoracic spinal neurons. We recorded the spontaneous and evoked activity of 45 dorsal horn neurons responsive to splanchnic stimulation before, during, and after chemical or electrical stimulation of the cervical spinal cord in chloralose-anesthetized spinal rats. Cervical spinal stimulation that inhibited RSA also inhibited the spontaneous and/or evoked activity of 44 dorsal horn neurons. In addition to inhibiting splanchnic-evoked neuronal responses, cervical stimulation also inhibited responses, in the same neurons, evoked by noxious heat or light brushing of receptive dermatomes. We concluded that cervical neurons participate in propriospinal inhibition of afferent transmission and that this inhibitory system may be involved in controlling the access of afferent information to SPNs.     

Thoracic visceral inputs use upper cervical segments to inhibit lumbar spinal neurons in rats

We tested the hypothesis that cardiopulmonary sympathetic afferent (CPSA) input entering upper thoracic spinal segments relays in the cervical spinal cord to inhibit activity of lumbar spinothalamic tract (STT) cells and dorsal horn (DH) cells. Two sequential spinal transections in the same animal were made, one at rostral C₁ and one at C₄–C₆ segments, to determine neuronal pathways involved in the inhibition. We concluded that inhibitory effects induced by CPSA and somatic stimulation might be mediated by propriospinal mechanisms located in upper cervical segments. Vagal inhibition required supraspinal pathways.     

Tonic descending modulation of spinal neurons with renal input.

Experiments were conducted to determine the influence of tonically active descending pathways on thoracolumbar spinal neurons that respond to renal nerve stimulation in anesthetized cats. We examined the effect of reversible blockade of spinal conduction on spontaneous activity, responses to renal nerve stimulation and responses to somatic stimuli of 71 spinal neurons. Mid-thoracic cold block resulted in enhanced responses (tonically inhibited neurons), reduced responses (tonically excited neurons), or did not affect neuronal responses. The spontaneous activity of 47 of 69 neurons (68%) increased from 7.3 +/- 2.0 spikes/s before cooling to 23.3 +/- 4.5 spikes/s during cooling. Activity of 8 neurons (12%) decreased while 14 (20%) had no change in activity. Cooling increased the responses of 51 of 71 neurons (72%) to renal nerve stimulation. Renal nerve stimulation evoked a two-fold increase in both short latency (early) and long latency (late) responses. Four neurons had a late response which was revealed by cold block. Cooling decreased responses of 8 of 71 neurons (11%) and 9 neurons (13%) were not affected. Cooling increased the early responses but decreased the late responses of 3 of 71 neurons (4%). All neurons had somatic receptive fields and 33 of 56 exhibited increased responses to somatic stimulation during cooling. In addition, receptive field sizes of 26 neurons increased. Four neurons had a decrease and 25 neurons had no change in receptive field size during cooling. These data indicate that tonically active descending pathways modulate the activity of most spinal neurons with renal input and the major effect of these pathways is inhibitory. This influence may be important in the modulation of spinal circuits that participate in reflexes evoked by renal afferent fibers.     

Afferent innervation of the trachea during postnatal development

Retrograde axonal transport of horseradish peroxidase was used in this study to determine the location and basic morphological parameters of neurons innervating the trachea in newborn, 10-, 20-, 30-day-old and 2-month-old kittens. Labeled neurons were detected in all animals in the nodose ganglion of the vagus nerve and in the spinal ganglia (C1-C7 and T1-T6 after injection of tracer into the cervical trachea, C5-C7 and T1-T8 with injection into the thoracic part of the trachea) from both sides. The content of vagal and spinal afferent neurons innervating the cervical part of trachea declined during development. The number of spinal afferent neurons with connections to the thoracic trachea did not change but the quantity of cells in nodose ganglion supplying the thoracic trachea increased from the moment of birth till 10 and 20 days and decreased later in postnatal development. In newborn, 10-day-old and 20-day-old animals, the largest number of afferent cells was connected with the cervical part of the trachea in comparison with the thoracic one, whereas in 2-month-old kittens the relation was opposite. We suggest that afferent innervation of the trachea is not morphologically complete at the moment of birth and does not become mature until the second month of life.     

Cardiopulmonary sympathetic afferent input to lower thoracic spinal neurons

Spinal neuronal responses to stimulation of cardiopulmonary sympathetic afferent (CPS) fibers were studied in 25 alpha-chloralose-anesthetized cats. Eighty-two neurons located in the T7-T9 segments were tested for responses to electrical stimulation of CPS fibers. Activity of 55 neurons was altered; 37 were excited, 10 were inhibited, and 8 were both excited and inhibited. All 55 cells with CPS input also responded to stimulation of somatic receptors and the left greater splanchnic nerve (SPL). Somatic receptive fields were primarily located on the upper portion of the abdomen and left lower rib cage. Short and long latency responses occurred following CPS and SPL stimulation. Latencies of responses to CPS stimulation were significantly longer than latencies of responses to SPL stimulation (P less than 0.05). Early responses to CPS stimulation were significantly less in magnitude compared to early responses to SPL stimulation (P less than 0.05). Cell responses to CPS stimulation were reduced in magnitude for as long as 300 ms when a conditioning stimulus was applied to SPL. Inhibitory responses of 10 cells to CPS fiber stimulation were best observed during repetitive stimulation. Eight of the cells were also inhibited by repetitive stimulation of SPL. Injection of bradykinin (4 micrograms/kg) into the left atrium increased activity of 16/30 cells from 8 +/- 2 to 22 +/- 5 spikes/s. The results demonstrate that CPS fiber stimulation alters activity of lower thoracic spinal neurons but not as intensely as SPL stimulation. These neurons may participate in cardiac-abdominal visceral reflexes or the pain of cardiac origin that is referred to the abdomen.     

Effects on Rats of Low Intensity and Frequency Electromagnetic Field Stimulation on Thoracic Spinal Neurons Receiving Noxious Cardiac and Esophageal Inputs

Objective Low intensity and low frequency electromagnetic field stimulation (EMFs) provides substantial pain relief in patients with various chronic pains. The aim of this study was to examine the effects of EMFs on the activity of thoracic spinal neurons responding to noxious visceral stimuli. Materials and Methods Extracellular potentials of single T₃–T₄ spinal neurons were recorded in pentobarbital anesthetized male rats. A catheter was placed in the pericardial sac to administer a mixture of algogenic chemicals for noxious cardiac stimulation (0.2 mL, 1 min). Noxious esophageal distension was produced by water inflation (0.4 mL, 20 sec) of a latex balloon. EMFs (0.839–0.952 Hz, 0.030–0.034 µG, 30–40 min) was applied with a pair of Helmholtz coils placed on both sides of the chest. Results After the onset of EMFs, excitatory neuronal responses to intrapericardial chemicals were reduced in 24/32 (75%) spinal neurons, increased in three neurons and were not affected in five neurons. The inhibitory effect on spinal neurons occurred 10–20 min after the onset of EMFs. Even after termination of EMFs, the suppression of spinal neuronal activity lasted for 1–2 hr. In contrast, excitatory responses of 7/18 (39%) neurons to esophageal distension were inhibited, five (28%) were excited and six (33%) were not affected by EMFs. Conclusions Results showed that EMFs generally reduced nociceptive responses of spinal neurons to noxious cardiac chemical stimuli, whereas it was not effective for nociceptive responses to esophageal mechanical stimulation.     

Proportion and location of spinal neurons receiving ventral root afferent inputs in the cat

Spinal neurons receiving ventral root afferent inputs were investigated in anesthetized and paralyzed cats. We were concerned with the afferent fibers in the ventral root that travel distally and then enter the spinal cord through the dorsal root. The questions to be answered included the proportion and distribution of spinal neurons receiving ventral root afferent inputs and their peripheral input characteristics. The 1.7 ventral root was cut near the spinal cord and the distal stump was stimulated while making a systematic search for neurons in the entire gray matter of the ipsilateral spinal cord that responded to the stimulation. The following conclusions were made: (i) the afferent fibers in the cat ventral root enter the spinal cord through the dorsal root and evoke a variety of responses (excitation, inhibition, or mixed) in a large proportion of spinal neurons (about 20%): (ii) these responses seem to be mediated largely by spinal mechanisms: (iii) spinal neurons receiving ventral root afferent inputs are situated in a wide region of the ventral spinal cord: (iv) ventral root fibers in a single root enter the spinal cord and exert their responses over a large region of the spinal cord (at least two spinal segments rostrally and caudally): (v) some of the spinal neurons that responded to ventral root stimulation were found to be ascending tract cells, suggesting that ventral root afferent inputs can reach supraspinal structures: (vi) ventral root afferent fibers converge onto spinal neurons that have a variety of peripheral receptive field characteristics: and (vii) with some exceptions, most neurons receiving ventral root inputs were excited best by mechanical and/or thermal noxious stimuli applied to the periphery.     

Descending modulation of thoracic visceroreceptive transmission by C1-C2 spinal neurons

Extracellular potentials of single T3 neurons were recorded in pentobarbital anesthetized male rats. Thoracic esophageal distension (ED, 0.3-0.4 ml, 20 s) and intrapericardial injection of bradykinin (BK, 10(-5) M, 0.2 ml, 1 min) were used as noxious visceral stimuli. Chemical activation of C1-C2 neurons with glutamate pledgets (1 M, 1-3 min) decreased background activity and/or excitatory responses of 26/35 (74%) neurons to ED and 34/44 (77%) neurons to BK. After spinal transection at rostral C1 in five animals, glutamate at C1-C2 still significantly reduced excitatory responses of five neurons to BK. Data showed that intraspinal descending modulation of C1-C2 neurons primarily produced descending inhibition of excitatory responses of thoracic spinal neurons to noxious visceral stimuli.