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Titolo:
In ovo chronic neurosteroid treatment affects the function and allosteric interactions of GABA(A) receptor modulatory sites
Autore:
Pignataro, L; de Plazas, SF;
Indirizzi:
Univ Buenos Aires, Fac Med, Inst Biol Celular & Neurociencias, RA-1121 Buenos Aires, DF, Argentina Univ Buenos Aires Buenos Aires DF Argentina RA-1121 Aires, DF, Argentina
Titolo Testata:
BRAIN RESEARCH
fascicolo: 1, volume: 902, anno: 2001,
pagine: 74 - 81
SICI:
0006-8993(20010525)902:1<74:IOCNTA>2.0.ZU;2-M
Fonte:
ISI
Lingua:
ENG
Soggetto:
CHICK OPTIC LOBE; MAMMALIAN CORTICAL-NEURONS; CENTRAL-NERVOUS-SYSTEM; BINDING-SITES; BENZODIAZEPINE RECEPTOR; RAT-BRAIN; AVIAN CNS; STEROID ANESTHETICS; A RECEPTOR; COMPLEX;
Keywords:
GABA(A) receptor; chloride channel; epipregnanolone chronic treatment; uncoupling; development; central nervous sytem (CNS);
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
35
Recensione:
Indirizzi per estratti:
Indirizzo: de Plazas, SF Univ Buenos Aires, Fac Med, Inst Biol Celular & Neurociencias, RA-1121 Buenos Aires, DF, Argentina Univ Buenos Aires Buenos Aires DF Argentina RA-1121 gentina
Citazione:
L. Pignataro e S.F. de Plazas, "In ovo chronic neurosteroid treatment affects the function and allosteric interactions of GABA(A) receptor modulatory sites", BRAIN RES, 902(1), 2001, pp. 74-81

Abstract

We investigated the effects of in ovo chronic administration of the endogenous neurosteroid epipregnanolone (5 beta -pregnan-3 beta -ol-20-one) on the GABA, receptor complex present in chick optic lobe synaptic membranes. Chronic epipregnanolone treatment failed to exert any effect on the chick optic lobe total protein content and wet weight at the different doses tested.[H-3]Flunitrazepam control binding remained unaltered after neurosteroid exposure, however, the positive allosteric modulation of this ligand by 4 muM allopregnanolone was reduced in a dose-dependent manner by neurosteroid treatment. Embryo exposure to 30 muM epipregnanolone decreased allopregnanolone EC50 and E-max values. Analyses of saturation binding isotherms disclosed that such administration had no effect on K-d and B-max values for [H-3]flunitrazepam and [H-3]GABA binding. [H-3]GABA binding modulation disclosedan increase in allopregnanolone EC50 value with a decrease in its E-max value. Diazepam EC50 and E-max values were enhanced, while low affinity sodium pentobarbital EC50 value was reduced by epipregnanolone treatment. The investigation of the GABA, receptor function revealed that administration of this neurosteroid reduces the efficacy of GABA to induce Cl-36 influx into microsacs prepared from chick optic lobe. These results indicate that endogenous neurosteroid epipregnanolone chronically administered in ovo produceshomologous uncoupling between steroid modulatory sites, and those corresponding to benzodiazepine and GABA receptors. Thus epipregnanolone is able toinduce heterologous changes in the allosteric linkage between benzodiazepine and barbiturate modulatory sites, and the GABA receptor site. Taken jointly with results on epipregnanolone enhancing effects on [H-3]flunitrazepamand [H-3]GABA binding, in the context of its endogenous synthesis, our present findings support this neurosteroid as the endogenous modulator of GABA, receptor sites and function during chick optic lobe development. (C) 2001Elsevier Science B.V. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 11/07/20 alle ore 17:07:03