Neuropeptide release in the spinal cord in response to noxious and non-noxious stimulation

Neuropeptides ◽  
1992 ◽  
Vol 22 (1) ◽  
pp. 19 ◽  
Author(s):  
A.W. Duggan
Keyword(s):  
Spinal Cord ◽  
Noxious Stimulation ◽  
Neuropeptide Release

Acetaminophen Inhibits Spinal Prostaglandin E2Release after Peripheral Noxious Stimulation 

1999 ◽  
Vol 91 (1) ◽  
pp. 231-239 ◽  
Author(s):  
Uta S. Muth-Selbach ◽  
Irmgard Tegeder ◽  
Kay Brune ◽  
Gerd Geisslinger
Keyword(s):  
Spinal Cord ◽  
Urinary Excretion ◽  
Dorsal Horn ◽  
Formalin Test ◽  
Intraperitoneal Administration ◽  
Noxious Stimulation ◽  
Cyclooxygenase Inhibitor ◽  
Nociceptive Processing ◽  
Pge2 Release

Background Prostaglandin play a pivotal role in spinal nociceptive processing. At therapeutic concentrations, acetaminophen is not a cyclooxygenase inhibitor. inhibitor. Thus, it is antinociceptive without having antiinflammatory or gastrointestinal toxic effects. This study evaluated the role of spinal prostaglandin E2 (PGE2) in antinociception produced by intraperitoneally administered acetaminophen. Methods The PGE2 concentrations in the dorsal horn of the spinal cord were measured after formalin was injected into the hind paw of rats. The effect of antinociceptive doses of acetaminophen (100, 200, and 300 mg/kg given intraperitoneally) on PGE2 levels and flinching behavior was monitored Spinal PGE2 and acetaminophen concentrations were obtained by microdialysis using a probe that was implanted transversely through the dorsal horn of the spinal cord at L4. Furthermore, the effects of acetaminophen on urinary prostaglandin excretion were determined. Results Intraperitoneal administration of acetaminophen resulted in a significant decrease in spinal PGE2 release that was associated with a significant reduction in the flinching behavior in the formalin test Acetaminophen was distributed rapidly into the spinal cord with maximum dialysate concentrations 4560 min after intraperitoneal administration. Urinary excretion of prostanoids (PGE2, PGF2alpha, and 6-keto-PGF1alpha) was not significantly altered after acetaminophen administration. Conclusions The data confirm the importance of PGE2 in spinal nociceptive processing. The results suggest that antinociception after acetaminophen administration is mediated, at least in part, by inhibition of spinal PGE2 release. The mechanism, however, remains unknown. The finding that urinary excretion of prostaglandins was not affected might explain why acetaminophen is antinociceptive but does not compromise renal safety.

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.

Response and receptive-field properties of spinomesencephalic tract cells in the cat

1986 ◽  
Vol 55 (1) ◽  
pp. 76-96 ◽  
Author(s):  
R. P. Yezierski ◽  
R. H. Schwartz
Keyword(s):  
Spinal Cord ◽  
Receptive Field ◽  
Dynamic Range ◽  
Receptive Fields ◽  
The Body ◽  
Noxious Stimulation ◽  
Primary Afferent ◽  
Receptive Field Properties ◽  
Afferent Fibers ◽  
Primary Afferent Fibers

Recordings were made from 90 identified spinomesencephalic tract (SMT) cells in the lumbosacral spinal cord of cats anesthetized with alpha-chloralose and pentobarbital sodium. Recording sites were located in laminae I-VIII. Antidromic stimulation sites were located in different regions of the rostral and caudal midbrain including the periaqueductal gray, midbrain reticular formation, and the deep layers of the superior colliculus. Twelve SMT cells were antidromically activated from more than one midbrain level or from sites in the medial thalamus. The mean conduction velocity for the population of cells sampled was 45.2 +/- 21.4 m/s. Cells were categorized based on their responses to graded intensities of mechanical stimuli and the location of excitatory and/or inhibitory receptive fields. Four major categories of cells were encountered: wide dynamic range (WDR); high threshold (HT); deep/tap; and nonresponsive. WDR and HT cells had excitatory and/or inhibitory receptive fields restricted to the ipsilateral hindlimb or extending to other parts of the body including the tail, forelimbs, and face. Some cells had long afterdischarges following noxious stimulation, whereas others had high rates of background activity that was depressed by nonnoxious and noxious stimuli. Deep/tap cells received convergent input from muscle, joint, or visceral primary afferent fibers. The placement of mechanical lesions at different rostrocaudal levels of the cervical spinal cord provided information related to the spinal trajectory of SMT axons. Six axons were located contralateral to the recording electrode in the ventrolateral/medial or lateral funiculi while two were located in the ventrolateral funiculus of the ipsilateral spinal cord. Stimulation at sites used to antidromically activate SMT cells resulted in the inhibition of background and evoked responses for 22 of 25 cells tested. Inhibitory effects were observed on responses evoked by low/high intensity cutaneous stimuli and by the activation of joint or muscle primary afferent fibers. Based on the response and receptive-field properties of SMT cells it is suggested that the SMT may have an important role in somatosensory mechanisms, particularly those related to nociception.

scholarly journals A brief period of moderate noxious stimulation induces hemorrhage and impairs locomotor recovery after spinal cord injury

2019 ◽  
Vol 212 ◽  
pp. 112695 ◽  
Author(s):  
Misty M. Strain ◽  
Michelle A. Hook ◽  
Joshua D. Reynolds ◽  
Yung-Jen Huang ◽  
Melissa K. Henwood ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Noxious Stimulation ◽  
Locomotor Recovery ◽  
Cord Injury

scholarly journals Propofol Action in Both Spinal Cord and Brain Blunts Electroencephalographic Responses to Noxious Stimulation in Goats

SLEEP ◽  
2001 ◽  
Vol 24 (1) ◽  
pp. 26-31 ◽  
Author(s):  
Joseph F Antognini ◽  
Jeffrey Saadi ◽  
Xiao Wei Wang ◽  
Earl Carstens ◽  
Marla Piercy
Keyword(s):  
Spinal Cord ◽  
Noxious Stimulation

Opiates modify induction of c-fos proto-oncogene in the spinal cord of the rat following noxious stimulation

1990 ◽  
Vol 111 (1-2) ◽  
pp. 46-51 ◽  
Author(s):  
T.R. Tölle ◽  
J.M. Castro-Lopes ◽  
A. Coimbra ◽  
W. Zieglgänsberger
Keyword(s):  
Spinal Cord ◽  
Noxious Stimulation

ELECTROACUPUNCTURE DECREASES C-FOS EXPRESSION IN THE SPINAL CORD INDUCED BY NOXIOUS STIMULATION OF THE RAT BLADDER

1998 ◽  
pp. 2274-2279 ◽  
Author(s):  
CARL J. CHANG ◽  
SHIH-TSUNG HUANG ◽  
KENNETH HSU ◽  
AUSTIN LIN ◽  
MARSHALL L. STOLLER ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Noxious Stimulation ◽  
Rat Bladder ◽  
Fos Expression ◽  
Stimulation Of

Intrathecal NSAIDS attenuate inflammation-induced neuropeptide release from rat spinal cord slices

Pain ◽  
1998 ◽  
Vol 78 (1) ◽  
pp. 39-48 ◽  
Author(s):  
D M. Southall ◽  
L R. Michael ◽  
R M. Vasko
Keyword(s):  
Spinal Cord ◽  
Rat Spinal Cord ◽  
Neuropeptide Release

Increasing Isoflurane from 0.9 to 1.1 Minimum Alveolar Concentration Minimally Affects Dorsal Horn Cell Responses to Noxious Stimulation 

1999 ◽  
Vol 90 (1) ◽  
pp. 208-214 ◽  
Author(s):  
Joseph F. Antognini ◽  
Earl Carstens
Keyword(s):  
Spinal Cord ◽  
Dorsal Horn ◽  
Minimum Alveolar Concentration ◽  
Neuronal Response ◽  
Spinal Cord Dorsal Horn ◽  
Noxious Stimulus ◽  
Lumbar Spinal Cord ◽  
Noxious Stimulation ◽  
Neuronal Responses ◽  
Cell Responses

Background The spinal cord appears to be the site at which isoflurane suppresses movement that occurs in response to a noxious stimulus. In an attempt to localize its site of suppressant action, the authors determined the effect of isoflurane on dorsal horn neuronal responses to supramaximal noxious stimulation at end-tidal concentrations that just permitted and just prevented movement. Methods Rats (n = 14) were anesthetized with isoflurane, and after lumbar laminectomy, the minimum alveolar concentration (MAC) for each rat was determined using a supramaximal mechanical stimulus. In these same rats, after extracellular microelectrode placement in the lumbar spinal cord, dorsal horn neuronal responses to the supramaximal stimulus were determined at the concentrations of isoflurane that bracketed each rat's MAC (0.1% higher and lower than MAC). The MAC of isoflurane was then re-determined. Results Dorsal horn neuronal response was 1,757+/-892 impulses/min at 0.9 MAC and 1,508+/-988 impulses/min at 1.1 MAC, a 14% decrease (P < 0.05). Cell responses varied, with some cells increasing their response at the higher concentration of isoflurane. The MAC of isoflurane was 1.38+/-0.2% before and 1.34+/-0.2% after determination of dorsal horn neuronal responses. Conclusions Isoflurane, at concentrations that bracket MAC, has a variable and minimal depressant effect on dorsal horn cell responses to noxious mechanical stimulation. These data suggest that the major action of isoflurane to suppress movement evoked by a noxious stimulus might occur primarily at a site other than the dorsal horn.

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