GABA(A) receptor subunit expression within hypophysiotropic CRH neurons: Adual hybridization histochemical study

Authors
Citation
We. Cullinan, GABA(A) receptor subunit expression within hypophysiotropic CRH neurons: Adual hybridization histochemical study, J COMP NEUR, 419(3), 2000, pp. 344-351
Citations number
47
Categorie Soggetti
Neurosciences & Behavoir
Journal title
JOURNAL OF COMPARATIVE NEUROLOGY
ISSN journal
00219967 → ACNP
Volume
419
Issue
3
Year of publication
2000
Pages
344 - 351
Database
ISI
SICI code
0021-9967(20000410)419:3<344:GRSEWH>2.0.ZU;2-T
Abstract
Dual hybridization histochemical studies were conducted to investigate the extent of colocalization of mRNA transcripts encoding the alpha 1-2 and bet a 1-3 subunits of the gamma aminobutyric acid (GABA), receptor with those f or corticotropin-releasing hormone (CRH) within the rat hypothalamic parave ntricular nucleus (PVN). A vast majority of CRH neurons (>94.5%) were found to express transcripts specific for the the alpha 2, beta 1 and beta 3 sub units; mRNAs for the alpha 1 and beta 2 subunits of the GABA(A) receptor we re detected within 53.3% and 65.7% of PVN CRH neurons, respectively. The re sults may have important implications for studies aimed at understanding GA BAergic influences upon the hypothalamic-pituitary-adrenocortical (HPA) axi s. Hypophysiotropic CRH neurons serve as the origin of the final common pat hway for glucocorticoid secretion in response to stressful stimuli, and GAB Aergic afferents have been implicated in afferent control of these neurons. The subunit composition of GABA(A) receptors at this key regulatory locus may affect the efficacy of a major inhibitory input, and thus the magnitude and/or duration of stress-induced glucocorticoid secretion. The present fi ndings reveal basal expression patterns of transcripts encoding several sub units of the GABA(A) receptor within stress-integrative CRH neurons, data w hich may be used to guide regulatory studies of GABAergic influences on the HPA axis under a variety of conditions. J. Comp. Neurol. 419:344-351, 2000 . (C) 2000 Wiley-Liss, Inc.