Splanchnic Input Research Articles

Gastric distension causes changes in heart rate and arterial blood pressure by affecting the crosstalk between vagal and splanchnic systems in anesthetised rats.

Various hindbrain nuclei have been demonstrated to be involved in the control of the cardiovascular reflexes elicited by both non-noxious and noxious gastric distension, through parasympathetic and sympathetic activation. The different role played by the branches of autonomic nervous system in exerting these effects and their crosstalk in relation to low-/high-pressure distension rate has not been examined yet. Therefore, in the present work, monolateral and bilateral vagotomy and splanchnicotomy were performed in anesthetised rats to analyse the involvement of hindbrain nuclei in haemodynamic changes caused by gastric distension at high (80mmHg) and low (15mmHg) pressure. The analysis of c-Fos expression in neuronal areas involved in cardiovascular control allowed us to examine their recruitment in response to various patterns of gastric distension and the crosstalk between vagal and splanchnic systems. The results obtained show that the low-pressure (non-noxious) gastric distension increases both heart rate and arterial blood pressure. In addition, the vagus nerve and hindbrain nuclei, such as nucleus ambiguous, ventrolateral medulla and lateral reticular nucleus, appear to be primarily involved in observed responses. In particular, we have found that although vagus nerve plays a central role in exerting those cardiovascular reflex changes at low gastric distension, for its functional expression an intact splanchnic system is mandatory. Hence, the absence of splanchnic input attenuates pressor responses or turns them into depressor responses. Instead at high-pressure (noxious) gastric distension, the splanchnic nerve represents the primary component in regulating the reflex cardiovascular effects.

The effects of clonidine and tizanidine on responses of nociceptive neurons in nucleus ventralis posterolateralis of the cat thalamus.

The effects of intravenous clonidine and tizanidine on nociceptive neurons in the nucleus ventralis posterolateralis (VPL) of the thalamus, a key station in the lateral system of ascending pain pathways, were evaluated in urethane-chloralose anesthetized cats. Intravenous clonidine and tizanidine produced a dose-dependent (5 and 10 micrograms/kg, and 25 and 50 micrograms/kg, respectively) suppression of responses of nociceptive specific (NS) and wide dynamic range (WDR) neurons in the VPL to high threshold splanchnic input. In contrast, the responses of both NS and WDR units to electrical stimulation of spinothalamic tract fibers in the ventrolateral funiculus (VLF) were little affected. We conclude that a site of suppressive action of the alpha 2-adrenoceptor agonists, as observed in nociceptive VPL neurons, is at the level of the spinal dorsal horn rather than in the VPL itself.

The Effects of Clonidine and Tizanidine on Responses of Nociceptive Neurons in Nucleus Ventralis Posterolateralis of the Cat Thalamus

The effects of intravenous clonidine and tizanidine on nociceptive neurons in the nucleus ventralis posterolateralis (VPL) of the thalamus, a key station in the lateral system of ascending pain pathways, were evaluated in urethane-chloralose anesthetized cats. Intravenous clonidine and tizanidine produced a dose-dependent (5 and 10 micro gram/kg, and 25 and 50 micro gram/kg, respectively) suppression of responses of nociceptive specific (NS) and wide dynamic range (WDR) neurons in the VPL to high threshold splanchnic input. In contrast, the responses of both NS and WDR units to electrical stimulation of spinothalamic tract fibers in the ventrolateral funiculus (VLF) were little affected. We conclude that a site of suppressive action of the alpha2-adrenoceptor agonists, as observed in nociceptive VPL neurons, is at the level of the spinal dorsal horn rather than in the VPL itself. (Anesth Analg 1995;81:259-64)

Processing of splanchnic and somatic input in thoracic spinal cord of the rat

To better understand the spinal transmission of visceral afferent information, we conducted neurophysiological studies of single spinal neurons that receive input from the greater splanchnic nerve (GSN). Extracellular single-neuron recordings were made in the thoracic spinal cord of chloralose-anesthetized, paralyzed, and artificially ventilated rats, some of which had undergone acute spinal transection at C1. Neurons were divided into four classes according to their responses to GSN stimulation: one-burst excitatory, two-burst excitatory, biphasic, and inhibited. We then studied the characteristics of the convergent somatic input to each class of neurons using either natural somatic stimuli or electrical stimulation of the iliohypogastric nerve (IHN). Most splanchnic input was mediated by unmyelinated fibers, whereas somatic input was mediated by both unmyelinated and small myelinated fibers. Most of the neurons exhibited somatic receptive fields, and the majority responded to both innocuous and noxious somatic stimuli. However, a small number could be excited only by GSN stimulation. Although a careful analysis of response characteristics indicated that there was a tendency for neurons to exhibit similar responses to electrical stimulation of the GSN and the IHN, we observed many combinations of somatic and visceral responses. We suggest that visceral afferent activity, in addition to being processed via convergent somatovisceral pathways, may be processed by neurons that convey only visceral information or by neurons in which visceral and somatic information is differentially coded.

Gastric vagal-evoked and greater splanchnic-evoked unitary responses in the hypothalamus

Gastric vagal and greater splanchnic nerve fibers were electrically stimulated to localize and characterize neuronal interactions in the hypothalamus of anesthetized cats. Extracellular recordings from 635 hypothalamic units were identified that responded to electrical stimulation of the left greater splanchnic nerve or gastric vagal fibers serving the proximal stomach. A total of 504 hypothalamic units in this group received input from both gastric vagal and greater splanchnic nerves. The gastric vagal-evoked hypothalamic (GVeH) and greater splanchnic-evoked hypothalamic (SeH) responses were widely distributed in the medial, paraventricular, and dorsomedial nuclei and lateral hypothalamus. The conduction velocity of the SeH response was significantly greater than the GVeH response. The latency of the SeH response showed two peaks [58 +/- 15.7 (SD) ms and 136 +/- 18.3 (SD) ms] indicating that the splanchnic input terminated on two different groups or populations of hypothalamic neurons. It also suggested that different pathways or fiber diameters in the pathway may be involved in the transmission of splanchnic input to the hypothalamus. The majority of the GVeH and SeH unitary responses were multiple spikes or short trains of action potentials. Excitatory and inhibitory responses were observed in tonically active hypothalamic units that responded to gastric vagal or greater splanchnic input. The duration of decreased excitability to gastric vagal or greater splanchnic input was significantly greater than the period of increased excitability. The condition-test paradigm was used to determine the time course of convergent gastric vagal-greater splanchnic input on single hypothalamic neurons.(ABSTRACT TRUNCATED AT 250 WORDS)

Parabrachial nucleus: neuronal evoked responses to gastric vagal and greater splanchnic nerve stimulation

Unitary responses were recorded extracellularly in the parabrachial nucleus (PBN) in anesthetized cats during electrical stimulation of the 1) gastric branches of the ventral and dorsal vagal trunks which serve the proximal stomach, and 2) left greater splanchnic nerve. The gastric vagally evoked parabrachial responses consisted of phasic single and multiple spike orthodromic discharges, which were bilaterally distributed, with a mean latency of 349 ms (S.D. ± 38.5). The parabrachial-evoked splanchnic unitary responses had a much shorter latency with a bimodal distribution (mean latencies, 53 and 128 ms, respectively). Convergence of gastric vagal input from the proximal stomach and the left greater splanchnic nerve upon single neurons in the PBN was electrophysiologically demonstrated in 132 units. Eighty-seven percent of the gastric vagally evoked parabrachial unitary responses were inhibited by simultaneous electrical stimulation of the splanchnic nerve. The condition-test paradigm was used to evaluate the time course of the splanchnic inhibition of the gastric vagally evoked parabrachial response. Reciprocal connections between neuronal populations in the nucleus tractus solitarius (NTS) which received gastric vagal input and the PBN were also identified electrophysiologically by direct microstimulation of the former structure. The density and characteristics of the gastric vagal and greater splanchnic input to the PBN suggested that this nucleus receives and processes a substantial amount of visceral afferent input. The PBN may serve as an important site for integrating visceral information governing the proximal stomach and ingestive processes.

Splanchnic input to thoracic spinal neurons and its supraspinal modulation in the rat

The unitary responses of 62 T 8–T 11 spinal neurons were recorded extracellularly following electrical stimulation of the greater splanchnic nerve (GSN) in chloralose-anesthetized rats. Recorded neurons were found inboth the dorsal and ventral horns. Fifty-seven neurons increased their firing rate in response to GSN stimulation; 8 of these exhibited biphasic responses consisting of excitations followed by inhibitions. Excitatory responses to GSN stimulation consisted of either one or two bursts with latencies consistent with activation by either Aδ or C fibers. GSN stimulation inhibited 5 neurons. The effects of reversible spinalization on spontaneous activity and on both synchronous and non-synchronous (afterdischarge) GSN-evoked responses were investigated using a cooling probe on the spinal cord between C 1 and C 2. Of 29 neurons tested in this way, 9 exhibited opposite directional changes in their spontaneous activities and their GSN-evoked responses upon spinalization. Differential effects of cold-block on first and second bursts, or on Aδ- and C-fiber mediated responses, were not usually observed. However, differential effects of cold-block on synchronous and non-synchronous portions of the overall GSN-evoked response were often observed in that their magnitudes often changed independently of one another. Supraspinal pathways contributed to GSN-evoked responses of several neurons because their responses were diminished during cooling while spontaneous activity was increased or unchanged. These decreases in the magnitude of the GSN-evoked response were not always accounted for by decreases in the synchronous portions of the responses. However, most neurons did exhibit decreases in the number of non-synchronous responses, or afterdischarges, during spinal cooling, exhibiting in some cases biphasic responses. This study provides evidence for strong supraspinal regulation of splanchnic afferent input to the spinal cord of the rat. Further, this regulation exhibits some specificity toward different portions of splanchnic-evoked responses in spinal neurons.

Units in tegmental nuclei responding to stimulation of gastric vagal and greater splanchnic fibers in the cat

The response of neurons in the ventral and dorsal tegmental nuclei during electrical stimulation of the gastric vagal fibers which serve the proximal stomach and the left greater splanchnic fibers were evaluated in chloralose-anesthetized cats. The mean latency of 181 gastric vagally evoked unitary responses recorded in the tegmental nuclei was 352.2 ms, whereas the latency of the left greater splanchnic-evoked tegmental response was significantly less (63.2 ms). The unitary responses to the gastric vagal and greater splanchnic fibers stimulation were bilaterally distributed in the ventral and dorsal tegmental nuclei. Convergence of the gastric vagal input from the proximal stomach and the left greater splanchnic input was observed in 151 units (83 percent). Stimulation of the greater splanchnic nerve usually resulted in a short latency excitation followed by an inhibitory effect on gastric vagally evoked responses. The results suggested that some convergent splanchnic inhibition of gastric vagally evoked responses was mediated via an interneuron. Projections from the nucleus tractus solitarius and the parabrachial nucleus to the tegmental nuclei were also identified electrophysiologically by direct microstimulation of the two former areas. The significant number of gastric vagal and splanchnic evoked unitary responses recorded in the ventral and dorsal tegmental nuclei suggested that they may serve as an important pontine site for processing of visceral information between the nucleus tractus solitarius and forebrain sites.

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.

Gastric vagal-splanchnic interactions in the brainstem of the cat

Brainstem unitary responses to gastric vagal-splanchnic nerve interactions were evaluated in anesthetized cats during electrical stimulation of the nerves. The gastric branches of the dorsal and ventral vagal trunks which serve the proximal stomach were electrically stimulated while recording in nucleus solitarius in the brainstem to identify evoked unitary responses. The vagally evoked brainstem responses were orthodromic in nature as evidenced by a slight variability in latency, reduction in the number of spikes upon decreasing stimulus strength and failure to follow higher stimulus frequencies. Interactions between gastric vagal input from the proximal stomach and left greater splanchnic nerve were evaluated by simultaneously stimulating the nerves electrically. Forty-three (16%) of the 265 gastric vagally evoked brainstem responses recorded were inhibited by simultaneously activating the left greater splanchnic nerve. The gastric vagally evoked responses inhibited by splanchnic input were nearly equally divided between the dorsal and ventral vagal trunks. Eighty-eight percent of those vagally evoked brainstem units inhibited by splanchnic input showed complete inhibition suggesting secure synaptic coupling. In addition, 3 gastric vagally activated brainstem units were identified which were also activated by greater splanchnic input. The latency of the splanchnic evoked brainstem response in these 3 units ranged from 55 to 89 ms compared to a mean latency of 290 ms (S.D.± 50ms) for the vagally evoked brainstem response. Splanchnic electrical stimulation usually produced an inhibitory effect upon the vagally evoked brainstem response which persisted for approximately 30 s following termination of splanchnic stimulation. This study identified single neurons in nucleus solitarius in the caudal brainstem of the cat which received: (1) excitatory input from gastric vagal fibers serving the proximal stomach, which travel in the dorsal and/or ventral vagal trunks; and (2) inhibitory input from fibers in the left greater splanchnic nerve. The gastric vagal-splanchnic brainstem interactions may be involved in receptive relaxation and gastric accomodation during ingestion.

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

Abstract Effects of electrical stimulation of the greater splanchnic nerves on T2–T4 spinal neurons were determined in 16 cats anesthetized with α-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 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 α-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.

Splanchnic nerve activation of single cells in the cat's postcruciate motorsensory cortex

Single neurons were recorded extracellularly in the forepaw posteruciate region, area 4 gamma, in chloralose-anesthetized cats. Several features of cellular behavior in response to skin and splanchnic nerve stimuli are described. First, in agreement with earlier work, the motor cortex receives bilateral, long-latency splanchnic input which depends primarily on A-delta afferents. Second, this input divides almost perfectly between the neuron populations delineated by Towe et al. on the basis of somatic responsiveness: sa (small-field) cells in this tissue do not receive splanchnic input, and m (wide-field) cells do. These data strengthen Towe's claim that the sa m dichotomy is fundamental and may offer a reliable identification routine for the two populations. Third, visceral input may be included as one of several long-latency excitation modes for cortical m neurons which do not involve the local sa cells: The body surface away from the contralateral topographic focus, the visual system, and the auditory system. Reasons are presented for assuming these diverse afferent systems to be based on A-delta fibers. Fourth, most pyramidal tract and some nonpyramidal tract neurons almost certainly receive splanchnic input, a finding which strengthens the notion of considerable intimacy between somatic and visceral control processes. Fifth, the common recruitment order previously shown for m neurons in response to stimmulation of skin areas other than the topographic focus obtains for their responsiveness to splanchnic stimulation as well. Finally, the suggestion is made that the several components of the wide-field input system to m neurons may have a major nociceptive function.