scholarly journals Somatic and visceral inputs to the thoracic spinal cord of the cat: effects of noxious stimulation of the biliary system

1983 ◽  
Vol 337 (1) ◽  
pp. 51-67 ◽  
Author(s):  
F. Cervero
Keyword(s):  
Spinal Cord ◽  
Biliary System ◽  
Noxious Stimulation ◽  
Thoracic Spinal Cord ◽  
Thoracic Spinal ◽  
Stimulation Of

Drastic Decrease in Isoflurane Minimum Alveolar Concentration and Limb Movement Forces after Thoracic Spinal Cooling and Chronic Spinal Transection in Rats

2005 ◽  
Vol 102 (3) ◽  
pp. 624-632 ◽  
Author(s):  
Steven L. Jinks ◽  
Carmen L. Dominguez ◽  
Joseph F. Antognini
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Minimum Alveolar Concentration ◽  
Tail Flick ◽  
Noxious Stimulation ◽  
Partial Recovery ◽  
Spinal Transection ◽  
Thoracic Spinal ◽  
Cord Injury ◽  
Stimulation Of

Background Individuals with spinal cord injury may undergo multiple surgical procedures; however, it is not clear how spinal cord injury affects anesthetic requirements and movement force under anesthesia during both acute and chronic stages of the injury. Methods The authors determined the isoflurane minimum alveolar concentration (MAC) necessary to block movement in response to supramaximal noxious stimulation, as well as tail-flick and hind paw withdrawal latencies, before and up to 28 days after thoracic spinal transection. Tail-flick and hind paw withdrawal latencies were measured in the awake state to test for the presence of spinal shock or hyperreflexia. The authors measured limb forces elicited by noxious mechanical stimulation of a paw or the tail at 28 days after transection. Limb force experiments were also conducted in other animals that received a reversible spinal conduction block by cooling the spinal cord at the level of the eighth thoracic vertebra. Results A large decrease in MAC (to </= 40% of pretransection values) occurred after spinal transection, with partial recovery (to approximately 60% of control) at 14-28 days after transection. Awake tail-flick and hind paw withdrawal latencies were facilitated or unchanged, whereas reflex latencies under isoflurane were depressed or absent. However, at 80-90% of MAC, noxious stimulation of the hind paw elicited ipsilateral limb withdrawals in all animals. Hind limb forces were reduced (by >/= 90%) in both chronic and acute cold-block spinal animals. Conclusions The immobilizing potency of isoflurane increases substantially after spinal transection, despite the absence of a baseline motor depression, or "spinal shock." Therefore, isoflurane MAC is determined by a spinal depressant action, possibly counteracted by a supraspinal facilitatory action. The partial recovery in MAC at later time points suggests that neuronal plasticity after spinal cord injury influences anesthetic requirements.

Myocardial ischemia induces the release of substance P from cardiac afferent neurons in rat thoracic spinal cord

2004 ◽  
Vol 286 (5) ◽  
pp. H1654-H1664 ◽  
Author(s):  
Fang Hua ◽  
Brian A. Ricketts ◽  
Angela Reifsteck ◽  
Jeffrey L. Ardell ◽  
Carole A. Williams
Keyword(s):  
Spinal Cord ◽  
Coronary Artery ◽  
Substance P ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Afferent Neurons ◽  
Thoracic Spinal Cord ◽  
Thoracic Spinal ◽  
Cardiac Afferents ◽  
Stimulation Of

Antibody-coated microprobes were inserted into the thoracic (T3–4) spinal cord in urethane-anesthetized Sprague-Dawley rats to detect the differences in the release of immunoreactive substance P-like (irSP) substances in response to differential activation of cardiac nociceptive sensory neurons (CNAN). CNAN were stimulated either by intrapericardial infusion of an inflammatory ischemic exudate solution (IES) containing algogenic substances (i.e., 10 mM each of adenosine, bradykinin, prostaglandin E2, and 5-hydroxytryptamine), or by transient occlusion of the left anterior descending coronary artery (CoAO). There was widespread basal release of irSP from the thoracic spinal cord. Stimulation of the CNAN by IES did not alter the pattern of release of irSP. Conversely, CoAO augmented the release of irSP from T3–4 spinal segments from laminae I–VII. This CoAO-induced irSP release was eliminated after thoracic dorsal rhizotomy. These results indicate that heterogeneous activation of cardiac afferents, as with focal coronary artery occlusion, represents an optimum input for activation of the cardiac neuronal hierarchy and for the resultant perception of angina. Excessive stimulation of cardiac nociceptive afferent neurons elicited during regional coronary artery occlusion involves the release of SP in the thoracic spinal cord and suggests that local spinal cord release of SP may be involved in the neural signaling of angina.

Effects of reversible spinalization on the visceral input to viscerosomatic neurons in the lower thoracic spinal cord of the cat

1986 ◽  
Vol 56 (3) ◽  
pp. 785-796 ◽  
Author(s):  
J. E. Tattersall ◽  
F. Cervero ◽  
B. M. Lumb
Keyword(s):  
Spinal Cord ◽  
Background Activity ◽  
Ventral Horn ◽  
Descending Inhibition ◽  
Thoracic Spinal Cord ◽  
Thoracic Spinal ◽  
Afferent Fibers ◽  
Biliary Pressure ◽  
Subcutaneous Tissues ◽  
Stimulation Of

Single-unit electrical activity has been recorded from 122 viscerosomatic neurons in the T9 and T11 segments of the cat's spinal cord. These neurons were excited by electrical and/or natural stimulation of visceral and somatic afferent fibers. The majority of viscerosomatic neurons (72%) received somatic nociceptive inputs, either exclusively or together with low-threshold somatic inputs. Many of these neurons were excited most strongly by intense mechanical stimulation of subcutaneous tissues, particularly by pinching or squeezing muscle. Twelve viscerosomatic neurons were excited by distensions of the biliary system at levels of biliary pressure greater than 25 mmHg. These intensities of biliary stimulation evoked transient increases in blood pressure, which suggest that the visceral stimuli were of nociceptive nature. The effects of reversible spinalization by cold block were tested on 98 viscerosomatic neurons. Three subgroups of viscerosomatic neurons were distinguished depending on whether their responses to visceral afferent stimulation were increased, decreased, or unchanged in the spinal state. Forty percent of all neurons tested increased the intensity of their responses to visceral stimulation in the spinal state. In addition, many of these neurons developed or increased their background activity and increased their somatic responses in the spinal state. It is concluded that these neurons were subjected to tonic descending inhibition of both somatic and visceral afferent inputs. More than 40% of the neurons in this group were located in or close to lamina V of the dorsal horn. In 44% of all neurons tested the response to visceral stimulation was reduced or abolished by spinalization. The background activity was not affected in the same manner and sometimes even increased during spinalization. The responses to somatic stimuli were fully tested in 11 neurons of this group and were found to be decreased, but not abolished, in nine neurons, unchanged in one cell, and increased in another one. Many of the neurons in this group were located in the ventral horn (laminae VII and VIII). Sixteen percent of all viscerosomatic neurons tested showed no change in their responses to visceral stimulation during spinalization. It is concluded that the visceral input to viscerosomatic neurons in the lower thoracic spinal cord is under considerable descending control, which includes excitation as well as tonic inhibition of visceral afferent information. This may represent part of the widespread effects of visceral nociceptive stimulation.

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

1994 ◽  
Vol 266 (1) ◽  
pp. R257-R267 ◽  
Author(s):  
E. W. Akeyson ◽  
L. P. Schramm
Keyword(s):  
Spinal Cord ◽  
Electrical Stimulation ◽  
Receptive Fields ◽  
Splanchnic Nerve ◽  
Careful Analysis ◽  
Thoracic Spinal Cord ◽  
Thoracic Spinal ◽  
Neurophysiological Studies ◽  
Somatic Input ◽  
Stimulation Of

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.

c-Fos expression in rat brain stem and spinal cord in response to activation of cardiac ischemia-sensitive afferent neurons and electrostimulatory modulation

2004 ◽  
Vol 287 (6) ◽  
pp. H2728-H2738 ◽  
Author(s):  
Fang Hua ◽  
Theresa Harrison ◽  
Chao Qin ◽  
Angela Reifsteck ◽  
Brian Ricketts ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Electrical Stimulation ◽  
Brain Stem ◽  
Nucleus Tractus Solitarius ◽  
Cardiac Ischemia ◽  
Afferent Neurons ◽  
Thoracic Spinal Cord ◽  
Thoracic Spinal ◽  
Afferent Fibers ◽  
Stimulation Of

The purpose of this study was to identify central neuronal sites activated by stimulation of cardiac ischemia-sensitive afferent neurons and determine whether electrical stimulation of left vagal afferent fibers modified the pattern of neuronal activation. Fos-like immunoreactivity (Fos-LI) was used as an index of neuronal activation in selected levels of cervical and thoracic spinal cord and brain stem. Adult Sprague-Dawley rats were anesthetized with urethane and underwent intrapericardial infusion of an “inflammatory exudate solution” (IES) containing algogenic substances that are released during ischemia (10 mM adenosine, bradykinin, prostaglandin E2, and 5-hydroxytryptamine) or occlusion of the left anterior descending coronary artery (CoAO) to activate cardiac ischemia-sensitive (nociceptive) afferent fibers. IES and CoAO increased Fos-LI above resting levels in dorsal horns in laminae I–V at C2 and T4 and in the caudal nucleus tractus solitarius. Dorsal rhizotomy virtually eliminated Fos-LI in the spinal cord as well as the brain stem. Neuromodulation of the ischemic signal by electrical stimulation of the central end of the left thoracic vagus excited neurons at the cervical and brain stem level but inhibited neurons at the thoracic spinal cord during IES or CoAO. These results suggest that stimulation of the left thoracic vagus excites descending inhibitory pathways. Inhibition at the thoracic spinal level that suppresses the ischemic (nociceptive) input signal may occur by a short-loop descending pathway via signals from cervical propriospinal circuits and/or a longer-loop descending pathway via signals from the nucleus tractus solitarius.

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