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Titolo:
EVIDENCE THAT THE PRESYNAPTIC A(2A)-ADENOSINE RECEPTOR OF THE RAT MOTOR-NERVE ENDINGS IS POSITIVELY COUPLED TO ADENYLATE-CYCLASE
Autore:
CORREIADESA P; RIBEIRO JA;
Indirizzi:
GULBENKIAN INST SCI,PHARMACOL LAB P-2781 OEIRAS PORTUGAL GULBENKIAN INST SCI,PHARMACOL LAB P-2781 OEIRAS PORTUGAL UNIV OPORTO,ICBAS,PHARMACOL LAB OPORTO PORTUGAL
Titolo Testata:
Naunyn-Schmiedeberg's archives of pharmacology
fascicolo: 5, volume: 350, anno: 1994,
pagine: 514 - 522
SICI:
0028-1298(1994)350:5<514:ETTPAR>2.0.ZU;2-9
Fonte:
ISI
Lingua:
ENG
Soggetto:
CYCLIC-NUCLEOTIDE PHOSPHODIESTERASE; TRANSMITTER RELEASE; ADENOSINE; FORSKOLIN; INHIBITOR; DITERPENE; SLICES; BRAIN; ACTIVATION; RMI-12330A;
Keywords:
CGS 21680C; FORSKOLIN; MDL 12,330A; ROLIPRAM; CYCLIC AMP STABLE ANALOGS; [H-3] ACETYLCHOLINE RELEASE; MOTOR NERVE TERMINALS; A(2A)-ADENOSINE RECEPTOR;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
36
Recensione:
Indirizzi per estratti:
Citazione:
P. Correiadesa e J.A. Ribeiro, "EVIDENCE THAT THE PRESYNAPTIC A(2A)-ADENOSINE RECEPTOR OF THE RAT MOTOR-NERVE ENDINGS IS POSITIVELY COUPLED TO ADENYLATE-CYCLASE", Naunyn-Schmiedeberg's archives of pharmacology, 350(5), 1994, pp. 514-522

Abstract

The action of the A(2a)-adenosine analogue, CGS 21680C, on electrically evoked [H-3]acetylcholine ([H-3]-ACh) release, and its interaction with forskolin (an activator of adenylate cyclase), MDL 12,330A (an irreversible inhibitor of adenylate cyclase), rolipram (an inhibitor of cyclic AMP specific phosphodiesterase), dibutyryl- (db-cAMP) and 8-bromo- (8-Br-cAMP) cyclic AMP analogues (substances that mimic intracellular actions of cyclic AMP), were investigated using rat phrenic nerve-hemidiaphragm preparations. CGS 21680C facilitated [H-3]-ACh release. Forskolin (but not 1,9-dideoxy forskolin), roLipram, db-cAMP and 8-Br-cAMP also increased evoked neurotransmitter release in a concentration-dependent manner. When the evoked [H-3]-ACh release that is dependenton stimulation of the adenylate cyclase/cyclic AMP transduction system was supramaximally stimulated by these compounds, CGS 21680C (3 nmol/l) could not further increase [H-3]-ACh release. Phosphodiesterase inhibition with low concentrations (less than or equal to 30 mu mol/l) of rolipram significantly potentiated the augmenting effect of CGS 21680C (1 nmol/l) on evoked [H-3]-ACh release. MDL 12,330A (an irreversible inhibitor of adenylate cyclase) decreased evoked [H-3]-ACh release. The irreversible blocking action of MDL 12,330A on [H-3]-ACh release was overcome by by-passing cyclase activation with db-cAMP and 8-Br-cAMP, but could not be overcome with FSK or CGS 21680C. The inhibitory effect of MDL 12,330A on evoked [H-3]-ACh release was not mimicked by nifedipine. It is concluded that the increase in [H-3]-ACh release caused by CGS 21680C results from activation of an A(2a)-adenosine receptorpositively linked to the adenylate cyclase/cyclic AMP system.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 05/04/20 alle ore 19:39:28