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Titolo:
Effects of pre- and postnatal corticosterone exposure on the rat hippocampal GABA system
Autore:
Stone, DJ; Walsh, JP; Sebro, R; Stevens, R; Pantazopolous, H; Benes, FM;
Indirizzi:
McLean Hosp, Mailman Res Ctr, Struct Neurosci Lab, Belmont, MA 02478 USA McLean Hosp Belmont MA USA 02478 ruct Neurosci Lab, Belmont, MA 02478 USA Harvard Univ, Sch Med, Dept Psychiat, Boston, MA 02115 USA Harvard Univ Boston MA USA 02115 Med, Dept Psychiat, Boston, MA 02115 USA Harvard Univ, Sch Med, Dept Neurol, Boston, MA 02115 USA Harvard Univ Boston MA USA 02115 h Med, Dept Neurol, Boston, MA 02115 USA Harvard Univ, Sch Med, Dept Neurosci, Boston, MA 02115 USA Harvard Univ Boston MA USA 02115 Med, Dept Neurosci, Boston, MA 02115 USA
Titolo Testata:
HIPPOCAMPUS
fascicolo: 5, volume: 11, anno: 2001,
pagine: 492 - 507
SICI:
1050-9631(2001)11:5<492:EOPAPC>2.0.ZU;2-Q
Fonte:
ISI
Lingua:
ENG
Soggetto:
GLUTAMIC-ACID DECARBOXYLASE; SUBUNIT MESSENGER-RNAS; ACUTE SWIM STRESS; BENZODIAZEPINE RECEPTOR-BINDING; CEREBRAL BLOOD-FLOW; PREFRONTAL CORTEX; A RECEPTOR; GENE-EXPRESSION; SEX-DIFFERENCES; PERINATAL COMPLICATIONS;
Keywords:
GAD; schizophrenia; GABA(A) receptor; benzodiazepine; mRNA; stress;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
78
Recensione:
Indirizzi per estratti:
Indirizzo: Benes, FM McLean Hosp, Mailman Res Ctr, Struct Neurosci Lab, 115 Mill St, Belmont, MA 02478 USA McLean Hosp 115 Mill St Belmont MA USA 02478 lmont, MA 02478 USA
Citazione:
D.J. Stone et al., "Effects of pre- and postnatal corticosterone exposure on the rat hippocampal GABA system", HIPPOCAMPUS, 11(5), 2001, pp. 492-507

Abstract

Several lines of evidence have implicated prenatal stress and the hippocampal GABA system in the pathophysiology of schizophrenia, and prenatal stress is believed to increase the risk for schizophrenia through alterations ofthis neurotransmitter. To explore this hypothesis, we treated male rats pre- and/or postnatally (P48 and P60) with either corticosterone (CORT) or vehicle to establish three study groups: VVV, receiving vehicle at all three time points; VCC, receiving vehicle prenatally and CORT at both postnatal timepoints; and CCC, receiving CORT at all three timepoints. Animals were sacrificed at either 24 h or 5 days after final injection and examined for mRNA levels of GAD(65), GAD(67), and the GABA, receptor subunits alpha (2) and gamma (2). At 24 h, GAD(65) mRNA was decreased in CA1, CA2, CA4, and dentate gyrus (DG) of VCC rats; this effect was either decreased or reversed inCCC-treated animals. No effect was detected in GAD67 mRNA at 24 h. At 5 days, CORT treatment increased GAD67 mRNA levels in CA1, CA3, and DG. Prenatal treatment with CORT was associated with increased responsiveness only in CA3 and DG. For the GABA(A) receptor, a. subunit mRNA did not show any change in response to CORT treatment, while that for the gamma (2) subunit was decreased in CA2 of both VCC- and CCC-treated animals. Consistent with gamma (2) subunit mRNA decreases, benzodiazepine (BZ) receptor binding activitywas decreased in CA2 with CORT treatment. Prenatal CORT exposure neither increased nor decreased this effect. These results demonstrate that CORT administration is associated with a complex regulation of mRNA expression for pre- and postnatal aspects of the hippocampal GABA system. Under these conditions, prenatal exposure to CORT may sensitize some of these effects, but does not fundamentally alter the nature of this response. (C) 2001 Wiley-Liss, Inc.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 23/01/20 alle ore 06:22:27