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Titolo:
CHRONIC OPIOID TREATMENT INDUCES ADENYLYL-CYCLASE-V SUPERACTIVATION -INVOLVEMENT OF G-BETA-GAMMA
Autore:
AVIDORREISS T; NEVO I; LEVY R; PFEUFFER T; VOGEL Z;
Indirizzi:
WEIZMANN INST SCI,DEPT NEUROBIOL IL-76100 REHOVOT ISRAEL WEIZMANN INST SCI,DEPT NEUROBIOL IL-76100 REHOVOT ISRAEL UNIV DUSSELDORF,DEPT PHYSIOL CHEM 2 D-40225 DUSSELDORF GERMANY
Titolo Testata:
The Journal of biological chemistry
fascicolo: 35, volume: 271, anno: 1996,
pagine: 21309 - 21315
SICI:
0021-9258(1996)271:35<21309:COTIAS>2.0.ZU;2-D
Fonte:
ISI
Lingua:
ENG
Soggetto:
ACTIVATED PROTEIN-KINASE; RAT-BRAIN; DEPENDENT ACTIVATION; CELL-LINES; RECEPTOR; EXPRESSION; CLONING; SUBUNITS; STIMULATION; MORPHINE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
63
Recensione:
Indirizzi per estratti:
Citazione:
T. Avidorreiss et al., "CHRONIC OPIOID TREATMENT INDUCES ADENYLYL-CYCLASE-V SUPERACTIVATION -INVOLVEMENT OF G-BETA-GAMMA", The Journal of biological chemistry, 271(35), 1996, pp. 21309-21315

Abstract

It has been known for some time that chronic treatment of neuronal cells and tissues with opioids, contrary to their acute effect, leads toan increase in cAMP accumulation. This phenomenon, defined as adenylyl cyclase superactivation, has been implicated in opiate addiction, yet the mechanism by which it is induced remains unclear. Here, we show that this phenomenon can be reproduced and studied in COS-7 cells cotransfected with adenylyl cyclase type V and mu-opioid receptor cDNAs. These cells display acute opioid inhibition of adenylyl cyclase activity, whereas prolonged exposure to the mu-agonist morphine or [D-Ala(2),N-methyl-Phe(4), Gly-ol(5)]enkephalin leads to a time-dependent superactivation of adenylyl cyclase. This superactivated state is reversible, because it is gradually lost following agonist withdrawal, Adenylylcyclase superactivation can be prevented by pertussis toxin pretreatment, indicating the involvement of G(i/o) proteins, or by cotransfection with the carboxyl terminus of beta-adrenergic receptor kinase or with alpha-transducin (scavengers of G(beta gamma) dimers), indicating arole for the G protein beta gamma dimers in adenylyl cyclase superactivation. However, contrary to several other G(beta gamma)-dependent signal transduction mechanisms (e.g. the extracellular signal-regulated kinase 2/MAP kinase pathway), adenylyl cyclase superactivation is not affected by the Has dominant negative mutant N17-Ras.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 15/07/20 alle ore 04:02:20