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Titolo:
FLUOXETINE INDUCES THE TRANSCRIPTION OF GENES ENCODING C-FOS, CORTICOTROPIN-RELEASING FACTOR AND ITS TYPE-1 RECEPTOR IN RAT-BRAIN
Autore:
TORRES G; HOROWITZ JM; LAFLAMME N; RIVEST S;
Indirizzi:
SUNY BUFFALO,DEPT PSYCHOL,BEHAV NEUROSCI PROGRAM BUFFALO NY 14260 CHU LAVAL,RES CTR,MOL ENDOCRINOL LAB QUEBEC CITY PQ G1V 4G2 CANADA UNIV LAVAL QUEBEC CITY PQ G1V 4G2 CANADA
Titolo Testata:
Neuroscience
fascicolo: 2, volume: 87, anno: 1998,
pagine: 463 - 477
SICI:
0306-4522(1998)87:2<463:FITTOG>2.0.ZU;2-7
Fonte:
ISI
Lingua:
ENG
Soggetto:
HYPOTHALAMIC PARAVENTRICULAR NUCLEUS; PITUITARY-ADRENOCORTICAL REGULATION; MESSENGER-RNA EXPRESSION; DEPRESSED-PATIENTS; IMMUNE CHALLENGE; BINDING-PROTEIN; CRF RECEPTORS; STRESS; SEROTONIN; ANTIDEPRESSANTS;
Keywords:
DEPRESSION; GENE EXPRESSION; HYPOTHALAMIC-PITUITARY-ADRENAL AXIS; PARAVENTRICULAR NUCLEUS; SEROTONIN; SEX DIFFERENCES;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
51
Recensione:
Indirizzi per estratti:
Citazione:
G. Torres et al., "FLUOXETINE INDUCES THE TRANSCRIPTION OF GENES ENCODING C-FOS, CORTICOTROPIN-RELEASING FACTOR AND ITS TYPE-1 RECEPTOR IN RAT-BRAIN", Neuroscience, 87(2), 1998, pp. 463-477

Abstract

Fluoxetine is a serotonin re-uptake blocker commonly used to treat endogenous depression. The present experiments were carried our to assess the effects of fluoxetine on c-fos induction throughout the rat brain. In addition, intron-directed in situ hybridization analysis was used to examine fluoxetine regulation of corticotropin-releasing factor heteronuclear gene transcription in the paraventricular nucleus of the hypothalamus. Because the actions of corticotropin-releasing factor are mediated by membrane bound corticotropin-releasing factor type 1 receptors, we also evaluated the stimulation of such receptors after acute fluoxetine exposure. The immediate-early gene, c-fos, was markedly induced in several telencephalic and diencephalic brain structures. Forinstance, a strong hybridized signal was apparent 30 min after fluoxetine (10 mg/kg; intraperitoneal) administration in the caudate putamen, septal nucleus, bed nucleus of stria terminalis, anterodorsal preoptic area, paraventricular nucleus. supraoptic nucleus, ventromedial hypothalamus and posterior hypothalamic nucleus. In addition, c-fos-expressing neurons were also evident in discrete amygdaloid nuclei. This nuclear induction was brief in duration, as levels of the immediate-early gene were mostly undetectable 90 min after drug administration. In contrast to the extensive induction of c-fos by fluoxetine throughout the brain parenchyma, elevation of corticotropin-releasing factor heteronuclear RNA levels were confined exclusively to neurosecretory nerve cells of the paraventricular nucleus, with peak levels detected 30 minafter fluoxetine exposure. Therefore, the time-course of corticotropin-releasing factor heteronuclear RNA closely paralleled that of c-fos. Significant changes in corticotropin-releasing factor type 1 receptormessenger RNA levels were also observed in the paraventricular nucleus but with a slow incremental biosynthesis of the receptor messenger RNA, as high levels were discernible only 360 min after fluoxetine treatment. Finally, we failed to detect sex-related differences in the acute response to fluoxetine, as both female and male rat brains showed acomparable induction of c-fos, corticotropin-releasing factor heteronuclear RNA and corticotropin-releasing Factor type 1 receptor expression within parvocellular neurosecretory nerve cells that govern the stress response. All of these findings are discussed in terms of specificsequences of nuclear events that couple fluoxetine-based serotonin input with changes in gene expression in selective neurons. (C) 1998 IBRO. Published by Elsevier Science Ltd.

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Documento generato il 20/09/20 alle ore 04:24:11