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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Role of the bed nucleus of the stria terminalis in the cardiovascular responses to acute restraint stress in rats

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Author(s):
Crestani, C. C. [1] ; Alves, F. H. F. [1] ; Tavares, R. F. [1] ; Correa, F. M. A. [1]
Total Authors: 4
Affiliation:
[1] Univ Sao Paulo, Sch Med Ribeirao Preto, Dept Pharmacol, BR-14049900 Sao Paulo - Brazil
Total Affiliations: 1
Document type: Journal article
Source: STRESS-THE INTERNATIONAL JOURNAL ON THE BIOLOGY OF STRESS; v. 12, n. 3, p. 268-278, 2009.
Web of Science Citations: 48
Abstract

The aim of this work was to test the hypothesis that the bed nucleus of the stria terminalis (BST) and noradrenergic neurotransmission therein mediate cardiovascular responses to acute restraint stress in rats. Bilateral microinjection of the non-specific synaptic blocker CoCl2 (0.1nmol/100nl) into the BST enhanced the heart rate (HR) increase associated with acute restraint without affecting the blood pressure increase, indicating that synapses within the BST influence restraint-evoked HR changes. BST pretreatment with the selective 1-adrenoceptor antagonist WB4101 (15nmol/100nl) caused similar effects to cobalt, indicating that local noradrenergic neurotransmission mediates the BST inhibitory influence on restraint-related HR responses. BST treatment with equimolar doses of the 2-adrenoceptor antagonist RX821002 or the -adrenoceptor antagonist propranolol did not affect restraint-related cardiovascular responses, reinforcing the inference that 1-adrenoceptors mediate the BST-related inhibitory influence on HR responses. Microinjection of WB4101 into the BST of rats pretreated intravenously with the anticholinergic drug homatropine methyl bromide (0.2mg/kg) did not affect restraint-related cardiovascular responses, indicating that the inhibitory influence of the BST on the restraint-evoked HR increase could be related to an increase in parasympathetic activity. Thus, our results suggest an inhibitory influence of the BST on the HR increase evoked by restraint stress, and that this is mediated by local 1-adrenoceptors. The results also indicate that such an inhibitory influence is a result of parasympathetic activation. (AU)