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Tytuł pozycji:

Delayed sympathetic dependence in the spared nerve injury (SNI) model of neuropathic pain

Tytuł :
Delayed sympathetic dependence in the spared nerve injury (SNI) model of neuropathic pain
Index Terms :
Animals Animals, Newborn Disease Models, Animal Ganglia, Spinal/drug effects/enzymology/pathology Guanethidine/administration & dosage/pharmacology Immunohistochemistry Male Neuralgia/metabolism/pathology/*physiopathology Pain Measurement Pain Threshold/drug effects Rats Rats, Sprague-Dawley Sciatic Nerve/injuries/metabolism/*physiopathology Spinal Cord/drug effects/metabolism/physiopathology Spinal Nerves/injuries/metabolism/*physiopathology Sympathectomy/methods Sympathetic Nervous System/*physiopathology Time Factors Tyrosine 3-Monooxygenase/metabolism
info:eu-repo/semantics/article
article
Wydawca :
2007
Dodane szczegóły :
Pertin, M.
Allchorne, A. J.
Beggah, A. T.
Woolf, C. J.
Decosterd, I.
Typ dokumentu :
Zasób elektroniczny
URL :
http://nbn-resolving.org/urn/resolver.pl?urn=urn:nbn:ch:serval-BIB_55C3A69E9B660">http://nbn-resolving.org/urn/resolver.pl?urn=urn:nbn:ch:serval-BIB_55C3A69E9B660
Dostępność :
Open access content. Open access content
info:eu-repo/semantics/openAccess
Copying allowed only for non-profit organizations
https://serval.unil.ch/disclaimer
Pozostałe numery :
CHLSR oai:serval.unil.ch:BIB_55C3A69E9B66
1008923752
Źródło wspomagające :
UNIV DE LAUSANNE-LETTRES,HIST,SCI RELG
From OAIster®, provided by the OCLC Cooperative.
Numer akcesji :
edsoai.on1008923752
Zasób elektroniczny
BACKGROUND: Clinical and experimental studies of neuropathic pain support the hypothesis that a functional coupling between postganglionic sympathetic efferent and sensory afferent fibers contributes to the pain. We investigated whether neuropathic pain-related behavior in the spared nerve injury (SNI) rat model is dependent on the sympathetic nervous system. RESULTS: Permanent chemical sympathectomy was achieved by daily injection of guanethidine (50 mg/kg s.c.) from age P8 to P21. SNI was performed at adulthood followed by 11 weeks of mechanical and thermal hypersensitivity testing. A significant but limited effect of the sympathectomy on SNI-induced pain sensitivity was observed. The effect was delayed and restricted to cold allodynia-like behavior: SNI-related cold scores were lower in the sympathectomized group compared to the control group at 8 and 11 weeks after the nerve injury but not before. Mechanical hypersensitivity tests (pinprick and von Frey hair threshold tests) showed no difference between groups during the study period. Concomitantly, pericellular tyrosine-hydroxylase immunoreactive basket structures were observed around dorsal root ganglia (DRG) neurons 8 weeks after SNI, but were absent at earlier time points after SNI and in sham operated controls. CONCLUSION: These results suggest that the early establishment of neuropathic pain-related behavior after distal nerve injury such as in the SNI model is mechanistically independent of the sympathetic system, whereas the system contributes to the maintenance, albeit after a delay of many weeks, of response to cold-related stimuli.

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