INVOLVEMENT OF THE BED NUCLEUS OF THE STRIA TERMINALIS IN TONIC REGULATION OF PARAVENTRICULAR HYPOTHALAMIC CRH AND AVP MESSENGER-RNA EXPRESSION

Citation
Jp. Herman et al., INVOLVEMENT OF THE BED NUCLEUS OF THE STRIA TERMINALIS IN TONIC REGULATION OF PARAVENTRICULAR HYPOTHALAMIC CRH AND AVP MESSENGER-RNA EXPRESSION, Journal of neuroendocrinology, 6(4), 1994, pp. 433-442
Citations number
41
Categorie Soggetti
Neurosciences,"Endocrynology & Metabolism
ISSN journal
09538194
Volume
6
Issue
4
Year of publication
1994
Pages
433 - 442
Database
ISI
SICI code
0953-8194(1994)6:4<433:IOTBNO>2.0.ZU;2-P
Abstract
The bed nucleus of the stria terminalis (BNST) occupies a central posi tion in pathways regulating hypothalamo-pituitary-adrenocortical (HPA) stress regulation. The potential role of the BNST in tonic neural con trol of HPA function was assessed by examining effects of selective BN ST lesions on expression of ACTH secretagogues in HPA-integrative neur ons of the medial parvocellular paraventricular nucleus. Anterior BNST lesions (ABN) involved major portions of the anteromedial, anterolate ral, ventromedial, ventrolateral, dorsolateral and juxtacapsular subnu clei. These lesions resulted in significant (30%) decreases in cortico tropin-releasing hormone (CRH) mRNA expression across the rostrocaudal extent of the medial parvocellular PVN, with no accompanying changes in basal arginine vasopressin (AVP) mRNA levels. Posterior BNST (PBN) lesions involved large but subtotal damage to the posterior intermedia te, posterior medial, posterior lateral and preoptic subnuclei; these lesions resulted in small but significant changes in CRH mRNA and slig ht increases in number of AVP mRNA-producing parvocellular neurons. PB N effects on CRH mRNA expression were most pronounced at the caudal ex tent of the medial parvocellular zone, suggesting a topographic input from the posterior BNST to the PVN that is only partially compromised by PBN lesions. Analysis of individual cases revealed a correlation be tween damage of the anterolateral BNST and decreased CRH mRNA levels, and damage of the posterior intermediate and/or posterior medial BNST and increased CRH mRNA levels. The results suggest differential BNST i nput into HPA regulation, perhaps reflecting the diversity of limbic i nput into the BNST region.