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Titolo:
Characterization of nociceptin/orphanin FQ-induced pain responses in conscious mice: Neonatal capsaicin treatment and N-methyl-D-aspartate receptor GluR epsilon subunit knockout mice
Autore:
Minami, T; Okuda-Ashitaka, E; Mori, H; Sakimura, K; Watanabe, M; Mishina, M; Ito, S;
Indirizzi:
Kansai Med Univ, Dept Med Chem, Moriguchi, Osaka 5708506, Japan Kansai MedUniv Moriguchi Osaka Japan 5708506 guchi, Osaka 5708506, Japan Osaka Med Coll, Dept Anesthesiol, Takatsuki, Osaka 5698686, Japan Osaka Med Coll Takatsuki Osaka Japan 5698686 atsuki, Osaka 5698686, Japan Niigata Univ, Inst Brain Res, Dept Cellular Neurobiol, Niigata 9518585, Japan Niigata Univ Niigata Japan 9518585 lar Neurobiol, Niigata 9518585, Japan Hokkaido Univ, Sch Med, Dept Anat, Sapporo, Hokkaido 0608638, Japan Hokkaido Univ Sapporo Hokkaido Japan 0608638 oro, Hokkaido 0608638, Japan Univ Tokyo, Sch Med, Dept Mol Neurobiol & Pharmacol, Tokyo 1130033, Japan Univ Tokyo Tokyo Japan 1130033 urobiol & Pharmacol, Tokyo 1130033, Japan
Titolo Testata:
NEUROSCIENCE
fascicolo: 1, volume: 97, anno: 2000,
pagine: 133 - 142
SICI:
0306-4522(2000)97:1<133:CONFPR>2.0.ZU;2-1
Fonte:
ISI
Lingua:
ENG
Soggetto:
CENTRAL-NERVOUS-SYSTEM; SUBSTANCE-P RELEASE; RAT SPINAL-CORD; OPIOID-RECEPTOR; ORPHANIN FQ/NOCICEPTIN; MESSENGER-RNA; INTRATHECAL MORPHINE; SENSORY NEURONS; DORSAL HORN; ENDOGENOUS LIGAND;
Keywords:
nociceptin/orphanin FQ; hyperalgesia; allodynia; capsaicin; substance P; NMDA receptor knockout mice;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
56
Recensione:
Indirizzi per estratti:
Indirizzo: Ito, S Kansai Med Univ, Dept Med Chem, Moriguchi, Osaka 5708506, Japan Kansai Med Univ Moriguchi Osaka Japan 5708506 Osaka 5708506, Japan
Citazione:
T. Minami et al., "Characterization of nociceptin/orphanin FQ-induced pain responses in conscious mice: Neonatal capsaicin treatment and N-methyl-D-aspartate receptor GluR epsilon subunit knockout mice", NEUROSCIENC, 97(1), 2000, pp. 133-142

Abstract

Activation of primary afferent C fibers gives rise to spinal release of substance P and glutamate, and these mediators facilitate the cascade of nociceptive processing. We recently showed that intrathecal administration of nociceptin or orphanin FQ thereafter called nociceptin) induced hyperalgesiato noxious thermal stimuli and allodynia to innocuous tactile stimuli applied to conscious mice. In the present study, we designed experiments to elucidate the pathways and mediators of nociceptin-evoked pain responses. Neonatal capsaicin treatment eliminated the induction of hyperalgesia and allodynia by nociceptin. Whereas this treatment markedly reduced the content of substance P in the spinal cord, it did not affect the nociceptin content orthe expression of nociceptin receptors and GluR epsilon and GluR xi subunits of N-methyl-D-aspartate receptors in it. The substance P antagonists CP96,345 and CP99,994 blocked the nociceptin-induced hyperalgesia, but not theallodynia. In contrast, the nociceptin-evoked allodynia, but not hyperalgesia, disappeared in N-methyl-D-aspaaate receptor GluR epsilon 1 subunit knockout mice. Both nociceptin-evoked hyperalgesia and allodynia were attenuated by morphine in a dose-dependent manner. Taken together, these results demonstrate that capsaicin-sensitive primary afferent fibers are involved notonly in thermal hyperalgesia but also in tactile allodynia induced by nociceptin, but in different pathways; the former is mediated by substance P and the latter is mediated by glutamate through the N-methyl-D-aspartate receptor comprising the GluR epsilon 1 subunit. (C) 2000 IBRO. Published by Elsevier Science Ltd.

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Documento generato il 29/03/20 alle ore 01:53:35