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Titolo:
SELECTIVE BLOCKADE OF A SLOWLY INACTIVATING POTASSIUM CURRENT IN STRIATAL NEURONS BY (+ -)6-CHLORO-APB HYDROBROMIDE (SKF82958)/
Autore:
NISENBAUM ES; MERMELSTEIN PG; WILSON CJ; SURMEIER DJ;
Indirizzi:
UNIV CONNECTICUT,DEPT PSYCHOL,U-20 STORRS CT 06269 UNIV TENNESSEE,COLL MED,DEPT NEUROBIOL & ANAT MEMPHIS TN 00000
Titolo Testata:
Synapse
fascicolo: 3, volume: 29, anno: 1998,
pagine: 213 - 224
SICI:
0887-4476(1998)29:3<213:SBOASI>2.0.ZU;2-I
Fonte:
ISI
Lingua:
ENG
Soggetto:
RAT NEOSTRIATAL NEURONS; PARKINSONIAN CYNOMOLGUS MONKEYS; SPINY PROJECTION NEURONS; D1 DOPAMINE RECEPTOR; ADENYLYL-CYCLASE; D-1; PROTEIN; AGONIST; DISEASE; CELLS;
Keywords:
I-D; SKF38393; SKF82958; CAMP; D-1 DOPAMINE RECEPTOR; PARKINSONS DISEASE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
37
Recensione:
Indirizzi per estratti:
Citazione:
E.S. Nisenbaum et al., "SELECTIVE BLOCKADE OF A SLOWLY INACTIVATING POTASSIUM CURRENT IN STRIATAL NEURONS BY (+ -)6-CHLORO-APB HYDROBROMIDE (SKF82958)/", Synapse, 29(3), 1998, pp. 213-224

Abstract

The ion channels of rat striatal neurons are known to be modulated bystimulation of D-1 dopamine receptors. The susceptibility of depolarization-activated K+ currents to be modulated by the D-1 agonist, llyl-1-phenyl-2,3,4,5-tetra-hydro-1H-3-benzazepine (APB) was investigated using whole-cell voltage-clamp recording techniques from acutely isolated neurons. APE (0.01-100 mu M) produced a concentration-dependent reduction in the total K+ current. At intermediate concentrations (ca. 10mu M), APE selectively depressed the slowly inactivating A-current (I-AS). A similar effect was produced by application of the D-1 agonist,roxy-1-phenyl-2,3,4,5-tetrahydro-1-H-2-benzazepine (SKF38393, 10 mu M). APB reduced I-AS rapidly, having onset and recovery time constants of 1.2 sec and 1.6 sec, respectively. Unexpectedly, the effect of APB could not be mimicked by application of Sp-adenosine 3',5'-cyclic monophosphothioate triethylamine (Sp-cAMPS, 100-200 mu M), a membrane-permeable analog of cyclic AMP (cAMP), or by pretreatment with forskolin (25 mu M), an activator of adenylyl cyclase. The reduction in IA, also was not blocked by pretreatment with the D-1 receptor antagonist, R(+)-SCH23390 hydrochloride (SCH23390, 10-20 mu M). In addition, intracellular dialysis with guanosine-5'-O-(2-thiodiphosphate(GDP-beta-S, 200 mu M) did not preclude the APE-induced inhibition of I-AS, nor did dialysis with guanosine-5'-O-(3-thiotriphosphate (GTP-gamma-S, 400 mu M) prevent reversal of the effect. The effect of APB was produced by a reduction in the maximal conductance of IA, without changing the voltage-dependence of the current. Collectively, these results argue that APE does not inhibit I-AS through D-1 receptors coupled to stimulation of adenylyl cyclase, but rather by allosterically regulating or blocking the channels giving rise to this current. (C) 1998 Wiley-Liss, Inc.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 28/03/20 alle ore 23:24:41