Hypothalamic supraoptic but not paraventricular nucleus is involved in cardiovascular responses to carbachol microinjected into the bed nucleus of stria terminalis of unanesthetized rats


Autoria(s): Alves, Fernando H. F.; Crestani, Carlos Cesar; Busnardo, Cristiane; Antunes-Rodrigues, Jose; Gomes, Felipe V.; Resstel, Leonardo B. M.; Correa, Fernando M. A.
Contribuinte(s)

Universidade Estadual Paulista (UNESP)

Data(s)

20/05/2014

20/05/2014

01/06/2011

Resumo

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Processo FAPESP: 10/09462-9

Processo FAPESP: 09/05308-8

Processo FAPESP: 10/17343-0

Microinjection of the cholinergic agonist carbachol into the bed nucleus of the stria terminalis (BST) has been reported to cause pressor response in unanesthetized rats, which was shown to be mediated by an acute release of vasopressin into the systemic circulation and followed by baroreflex-mediated bradycardia. In the present study, we tested the possible involvement of the hypothalamic paraventricular (PVN) and supraoptic (SON) nuclei in the pressor response evoked by carbachol microinjection into the BST of unanesthetized rats. For this, cardiovascular responses following carbachol (1 nmol/100 nL) microinjection into the BST were studied before and after PVN or SON pretreatment, either ipsilateral or contralateral in relation to BST microinjection site, with the nonselective neurotransmission blocker cobalt chloride (CoCl(2), 1 mM/100 nL). Carbachol microinjection into the BST evoked pressor response. Moreover, BST treatment with carbachol significantly increased plasma vasopressin levels, thus confirming previous evidences that carbachol microinjection into the BST evokes pressor response due to vasopressin release into the circulation. SON pretreatment with CoCl(2), either ipsilateral or contralateral in relation to BST microinjection site, inhibited the pressor response to carbachol microinjection into the BST. However, CoCl(2) microinjection into the ipsilateral or contralateral PVN did not affect carbachol-evoked pressor response. In conclusion, our results suggest that pressor response to carbachol microinjection into the BST is mediated by SON magnocellular neurons, without significant involvement of those in the PVN. The results also indicate that responses to carbachol microinjection into the BST are mediated by a neural pathway that depends on the activation of both ipsilateral and contralateral SON. (C) 2011 Elsevier B.V. All rights reserved.

Formato

31-43

Identificador

http://dx.doi.org/10.1016/j.brainres.2011.03.067

Brain Research. Amsterdam: Elsevier B.V., v. 1393, p. 31-43, 2011.

0006-8993

http://hdl.handle.net/11449/8130

10.1016/j.brainres.2011.03.067

WOS:000291380300004

WOS000291380300004.pdf

Idioma(s)

eng

Publicador

Elsevier B.V.

Relação

Brain Research

Direitos

openAccess

Palavras-Chave #Cholinergic neurotransmission #BST #Hypothalamus #Vasopressin #Heart rate and arterial pressure
Tipo

info:eu-repo/semantics/article