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Titolo:
INVOLVEMENT OF SEROTONERGIC PATHWAYS IN MEDIATING THE NEURONAL-ACTIVITY AND GENETIC TRANSCRIPTION OF NEUROENDOCRINE CORTICOTROPIN-RELEASINGFACTOR IN THE BRAIN OF SYSTEMICALLY ENDOTOXIN-CHALLENGED RATS
Autore:
LAFLAMME N; FEUVRIER E; RICHARD D; RIVEST S;
Indirizzi:
CHU LAVAL,RES CTR,MOL ENDOCRINOL LAB,2705 BLVD LAURIER QUEBEC CITY PQG1V 4G2 CANADA CHU LAVAL,RES CTR,MOL ENDOCRINOL LAB QUEBEC CITY PQ G1V 4G2 CANADA UNIV LAVAL,DEPT ANAT & PHYSIOL QUEBEC CITY PQ G1V 4G2 CANADA
Titolo Testata:
Neuroscience
fascicolo: 1, volume: 88, anno: 1999,
pagine: 223 - 240
SICI:
0306-4522(1999)88:1<223:IOSPIM>2.0.ZU;2-Z
Fonte:
ISI
Lingua:
ENG
Soggetto:
PITUITARY-ADRENOCORTICAL AXIS; 5-HT1A RECEPTOR AGONISTS; INDUCED ACTIVATION; ADRENAL AXIS; C-FOS; SYMPATHOADRENOMEDULLARY SYSTEM; INTRAVENOUS LIPOPOLYSACCHARIDE; INTERLEUKIN-1 RECEPTOR; BACTERIAL-ENDOTOXIN; SECRETION;
Keywords:
ACUTE-PHASE RESPONSE; CORTICOTROPH AXIS; IMMEDIATE-EARLY GENES; LIPOPOLYSACCHARIDE; NEUROENDOCRINOLOGY; PARA-CHLOROPHENYLALANINE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
61
Recensione:
Indirizzi per estratti:
Citazione:
N. Laflamme et al., "INVOLVEMENT OF SEROTONERGIC PATHWAYS IN MEDIATING THE NEURONAL-ACTIVITY AND GENETIC TRANSCRIPTION OF NEUROENDOCRINE CORTICOTROPIN-RELEASINGFACTOR IN THE BRAIN OF SYSTEMICALLY ENDOTOXIN-CHALLENGED RATS", Neuroscience, 88(1), 1999, pp. 223-240

Abstract

The present study investigated the effect of serotonin depletion on the neuronal activity and transcription of corticotropin-releasing factor in the rat brain during the acute-phase response. Conscious male rats received an intraperitoneal (i.p.) injection with the immune activator lipopolysaccaride (25 mu g/100 g body wt) after being treated for three consecutive days with para-chlorophenylalanine (30mg/100g/day). This irreversible inhibitor of tryptophane-5-hydroxylase decreased hypothalamic serotonin levels by 96%. One, 3 and 6h after a single i.p, injection of lipopolysaccharide or vehicle solution, rats were killed and their brains cut in 30-mu m coronal sections. Messenger RNAs encoding c-fos, nerve-growth factor inducible-B gene, corticotropin-releasing factor and the heteronuclear RNA encoding corticotropin-releasing factor primary transcript were assayed by in situ hybridization using S-35-labeled riboprobes, whereas Fos-immunoreactive nuclei were labeled by immunocytochemistry. Lipopolysaccharide induced a wide neuronal activation indicated by the expression of both immediate-early gene transcripts and Fos protein in numerous structures of the brain. The signalfor both immediate-early gene transcripts was low to moderate Ih after lipopolysaccharide administration, maximal at 3 h and decline at 6 hpost-injection, whereas at that time, Fos-immunoreactive nuclei were still detected in most of the c-fos messenger RNA-positive structures. Interestingly, the strong and widespread induction of both immediate-early gene transcripts was almost totally inhibited by para-chlorophenylalanine treatment; in the hypothalamic paraventricular nucleus for example, c-Sos messenger RNA signal and the number of Fos-immunoreactive positive cells were reduced by 80 and 48%, respectively, in serotonin-depleted rats treated with the bacterial endotoxin. This blunted neuronal response was also associated with an attenuated stimulation of neuroendocrine corticotropin-releasing factor transcription and plasma corticosterone release. Indeed, lipopolysaccharide caused a selective expression of corticotropin-releasing factor primary transcript in theparaventricular nucleus of the hypothalamus and this effect was si,significantly reduced by treatment with the serotonin inhibitor. However, basal expression of corticotropin-releasing factor messenger RNA across the brain (bed nucleus of the stria terminalis, medial preoptic area, paraventricular nucleus of the hypothalamus, central nucleus of the amygdala, etc.) was not affected by the para-chlorophenylalanine treatment. These results suggest that the integrity of serotonin pathwaysplays a role in the neuronal activity triggered by the systemic endotoxin insult. The fact that serotonin depletion largely prevented activation of neurosecretory parvocellular neurons of the paraventricular nucleus of the hypothalamus and neuroendocrine corticotropin-releasing factor gene transcription in response to immunogenic challenge provides the evidence that serotonergic system is part of the brain circuitryinvolved in the corticotroph axis-immune interface. (C) 1998 IBRO. Published by Elsevier Science Ltd.

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Documento generato il 28/11/20 alle ore 18:47:37