Key role for the epsilon isoform of protein kinase C in painful alcoholic neuropathy in the rat.
J Neurosci
; 20(22): 8614-9, 2000 Nov 15.
Article
em En
| MEDLINE
| ID: mdl-11069970
ABSTRACT
Chronic alcohol consumption produces a painful peripheral neuropathy for which there is no reliably successful therapy, attributable to, in great part, a lack of understanding of the underlying mechanisms. We tested the hypothesis that neuropathic pain associated with chronic alcohol consumption is a result of abnormal peripheral nociceptor function. In rats maintained on a diet to simulate chronic alcohol consumption in humans, mechanical hyperalgesia was present by the fourth week and maximal at 10 weeks. Thermal hyperalgesia and mechanical allodynia were also present. Mechanical threshold of C-fibers in ethanol fed rats was lowered, and the number of action potentials during sustained stimulation increased. The hyperalgesia was acutely attenuated by intradermal injection of nonselective protein kinase C (PKC) or selective PKCepsilon inhibitors injected at the site of nociceptive testing. Western immunoblot analysis indicated a higher level of PKCepsilon in dorsal root ganglia from alcohol-fed rats, supporting a role for enhanced PKCepsilon second-messenger signaling in nociceptors contributing to alcohol-induced hyperalgesia.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Proteína Quinase C
/
Neuropatia Alcoólica
/
Gânglios Espinais
/
Isoenzimas
Limite:
Animals
Idioma:
En
Revista:
J Neurosci
Ano de publicação:
2000
Tipo de documento:
Article
País de afiliação:
Estados Unidos