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Titolo:
Chronic morphine treatment alters NMDA receptor-mediated synaptic transmission in the nucleus accumbens
Autore:
Martin, G; Ahmed, SH; Blank, T; Spiess, J; Koob, GF; Siggins, GR;
Indirizzi:
Scripps Clin & Res Fdn, Res Inst, Dept Neuropharmacol, La Jolla, CA 92037 USA Scripps Clin & Res Fdn La Jolla CA USA 92037 acol, La Jolla, CA 92037 USA Max Planck Inst Expt Med, Dept Mol Neuroendocrinol, D-3400 Gottingen, Germany Max Planck Inst Expt Med Gottingen Germany D-3400 400 Gottingen, Germany
Titolo Testata:
JOURNAL OF NEUROSCIENCE
fascicolo: 20, volume: 19, anno: 1999,
pagine: 9081 - 9089
SICI:
0270-6474(19991015)19:20<9081:CMTANR>2.0.ZU;2-M
Fonte:
ISI
Lingua:
ENG
Soggetto:
D-ASPARTATE RECEPTOR; CHRONIC ETHANOL TREATMENT; SUBUNIT MESSENGER-RNA; RAT-BRAIN; HIPPOCAMPAL-NEURONS; ANALGESIC TOLERANCE; WITHDRAWAL SYMPTOMS; OPIATE TOLERANCE; UP-REGULATION; EXPRESSION;
Keywords:
NMDA glutamate receptors; electrophysiology; phorbol ester; protein kinase C; chronic morphine treatment; kinetics;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
64
Recensione:
Indirizzi per estratti:
Indirizzo: Siggins, GR Scripps Clin & Res Fdn, Res Inst, Dept Neuropharmacol, CVN-12,10550 N Torrey Pines Rd, La Jolla, CA 92037 USA Scripps Clin & Res Fdn CVN-12,10550 N Torrey Pines Rd La Jolla CA USA 92037
Citazione:
G. Martin et al., "Chronic morphine treatment alters NMDA receptor-mediated synaptic transmission in the nucleus accumbens", J NEUROSC, 19(20), 1999, pp. 9081-9089

Abstract

In a study of a possible substrate underlying morphine addiction, we examined NMDA receptor-mediated synaptic transmission of core nucleus accumbens neurons after chronic morphine treatment, using intracellular recording in a slice preparation of rat. We evoked pharmacologically isolated NMDA EPSCsby local stimulation and elicited inward currents by NMDA superfusion. In control slices, Mg2+ and phorbol 12,13-diacetate (PDAc), a protein kinase Cactivator, strongly inhibited and increased, respectively, NMDA EPSC amplitudes. The PDAc effects were likely postsynaptic because PDAc enhanced the currents evoked by superfused NMDA to the same extent that it did the NMDA EPSCs. Chronic morphine treatment significantly decreased NMDA EPSC amplitudes and the sensitivity of NMDA EPSCs to Mg2+ and PDAc, as well as the kinetics of the decay (inactivation rate) of the EPSCs (from 97 +/- 2.5 msec inuntreated rats to 78.7 +/- 1.8 msec in slices from treated rats). One weekafter withdrawal, the Mg2+ and PDAc effects were still significantly less than those in control slices. Interestingly, 1 week of withdrawal led to anincreased NMDA EPSC inactivation rate compared with controls. These data demonstrate that chronic morphine treatment significantly alters NMDA receptor-mediated synaptic transmission in the accumbens, and these effects persist 1 week after withdrawal. These long-term effects may represent an important neuroadaptation in opiate dependence.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 29/03/20 alle ore 01:41:00