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Titolo:
ADENYLYLCYCLASE SUPERSENSITIZATION IN MU-OPIOID RECEPTOR-TRANSFECTED CHINESE-HAMSTER OVARY CELLS FOLLOWING CHRONIC OPIOID TREATMENT
Autore:
AVIDORREISS T; BAYEWITCH M; LEVY R; MATUSLEIBOVITCH N; NEVO I; VOGEL Z;
Indirizzi:
WEIZMANN INST SCI,DEPT NEUROBIOL IL-76100 REHOVOT ISRAEL WEIZMANN INST SCI,DEPT NEUROBIOL IL-76100 REHOVOT ISRAEL
Titolo Testata:
The Journal of biological chemistry
fascicolo: 50, volume: 270, anno: 1995,
pagine: 29732 - 29738
SICI:
0021-9258(1995)270:50<29732:ASIMRC>2.0.ZU;2-8
Fonte:
ISI
Lingua:
ENG
Soggetto:
GLIOMA HYBRID-CELLS; ADENYLATE-CYCLASE ACTIVITY; NEUROBLASTOMA SH-SY5Y CELLS; NUCLEOTIDE-BINDING-PROTEINS; PHARMACOLOGICAL PROPERTIES; SENSORY NEURONS; CYCLIC-AMP; TOLERANCE; EXPRESSION; INHIBITION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
47
Recensione:
Indirizzi per estratti:
Citazione:
T. Avidorreiss et al., "ADENYLYLCYCLASE SUPERSENSITIZATION IN MU-OPIOID RECEPTOR-TRANSFECTED CHINESE-HAMSTER OVARY CELLS FOLLOWING CHRONIC OPIOID TREATMENT", The Journal of biological chemistry, 270(50), 1995, pp. 29732-29738

Abstract

Using CRO cells stably transfected with rat mu-opioid receptor cDNA, we show that the mu-agonists morphine and [D-Ala(2),N-methyl-Phe(4),Gly-ol(5)]enkephalin are negatively coupled to adenylylcyclase and inhibit forskolin-stimulated cAMP accumulation. Chronic exposure of cells to morphine leads to the rapid development of tolerance. Withdrawal of morphine or [D-Ala(2),N-methyl-Phe(4),Gly-ol(5)]enkephalin following chronic treatment (by wash or addition of the antagonist naloxone) leads to an immediate increase in cyclase activity (supersensitization or overshoot), which is gradually reversed upon further incubation with naloxone. Phosphodiesterase inhibitors do not affect the overshoot, indicating that it results from cyclase stimulation rather than phosphodiesterase regulation, Morphine's potency to inhibit cAMP accumulation is the same before and after chronic treatment, suggesting that the apparent tolerance results from cyclase activation, rather than from receptor desensitization. The similar kinetics of induction of tolerance and overshoot support this idea. Both the overshoot and acute opioid-induced cyclase inhibition are blocked by naloxone and are pertussis toxin-sensitive, indicating that both phenomena are mediated by the mu-receptor and G(i)/G(o) proteins. The supersensitization is cycloheximide-insensitive, indicating that it does not require newly synthesized proteins. This is supported by the rapid development of supersensitization. Taken together, these results show that mu-transfected cells can serve as a model for investigating molecular and cellular mechanisms underlying opiate drug addiction.

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Documento generato il 10/07/20 alle ore 01:53:33