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(Referência obtida automaticamente do Web of Science, por meio da informação sobre o financiamento pela FAPESP e o número do processo correspondente, incluída na publicação pelos autores.)

Dissociation in control of physiological and behavioral responses to emotional stress by cholinergic neurotransmission in the bed nucleus of the stria terminalis in rats

Texto completo
Autor(es):
Gouveia, Marianna K. [1] ; Miguel, Tarciso T. [2] ; Busnardo, Cristiane [3] ; Scopinho, America A. [3] ; Correa, Fernando M. A. [3] ; Nunes-de-Souza, Ricardo L. [4, 1] ; Crestani, Carlos C. [4, 1]
Número total de Autores: 7
Afiliação do(s) autor(es):
[1] Univ Estadual Paulista UNESP, Sch Pharmaceut Sci, Pharmacol Lab, Araraquara, SP - Brazil
[2] Fed Univ Uberlandia UFU, Inst Biomed Sci, Uberlandia, MG - Brazil
[3] Univ Sao Paulo, Sch Med Ribeirao Preto, Dept Pharmacol, BR-14049 Ribeirao Preto - Brazil
[4] Joint UFSCar UNESP Grad Program Physiol Sci, Sao Carlos, SP - Brazil
Número total de Afiliações: 4
Tipo de documento: Artigo Científico
Fonte: Neuropharmacology; v. 101, p. 379-388, FEB 2016.
Citações Web of Science: 8
Resumo

The bed nucleus of the stria terminalis (BNST) is a forebrain structure implicated in physiological and behavioral responses to emotional stress. However, the local neurochemical mechanisms mediating the BNST control of stress responses are not fully known. Here, we investigated the involvement of BNST cholinergic neurotransmission, acting via muscarinic receptors, in cardiovascular (increase in blood pressure and heart rate and fall in tail skin temperature) and neuroendocrine (increase in plasma corticosterone) responses and behavioral consequences (anxiogenic-like effect in the elevated plus-maze) evoked by acute restraint stress in rats. Bilateral microinjection into the BNST of either the choline uptake inhibitor hemicholinium-3 (3 nmol/100 nl) or the muscarinic receptor antagonist methylatropine (3 nmol/100 nl) enhanced the heart rate increase and inhibited the anxiogenic-like effect observed in the elevated plus-maze evoked by restraint. However, neither hemicholinium-3 nor methylatropine affected the increase in blood pressure and plasma corticosterone levels and the fall in tail skin temperature. Facilitation of local cholinergic signaling by microinjection of the acetylcholinesterase inhibitor neostigmine (0.1 nmol/100 nl) into the BNST reduced restraint-evoked pressor and tachycardiac responses and the fall in tail cutaneous temperature, without affecting the increase in plasma corticosterone. All effects of neostigmine were completely abolished by local BNST pretreatment with methylatropine. These findings indicate an opposite role of BNST cholinergic neurotransmission, acting via local muscarinic receptor, in control of cardiovascular responses (inhibitory influence) and emotional consequences (facilitatory influence) evoked by restraint stress. Furthermore, present findings provide evidence that BNST control of neuroendocrine responses to stress is mediated by mechanisms others than local cholinergic signaling. (C) 2015 Elsevier Ltd. All rights reserved. (AU)

Processo FAPESP: 12/14376-0 - Comparação do efeito de dois protocolos de estresse crônico sobre a função cardiovascular e autonômica em ratos
Beneficiário:Carlos Cesar Crestani
Modalidade de apoio: Auxílio à Pesquisa - Regular
Processo FAPESP: 12/50549-6 - Envolvimento da neurotransmissão colinérgica no núcleo leito da estria terminal nas respostas autonômicas, neuroendócrinas e comportamentais desencadeadas pelo estresse por restrição agudo em ratos
Beneficiário:Carlos Cesar Crestani
Modalidade de apoio: Auxílio à Pesquisa - Regular
Processo FAPESP: 13/01283-6 - Sistema hierárquico de defesa no camundongo: modulação pelo fator de liberação de corticotrofina (CRF)
Beneficiário:Ricardo Luiz Nunes de Souza
Modalidade de apoio: Auxílio à Pesquisa - Regular
Processo FAPESP: 15/05922-9 - Estudo da participação da neurotransmissão CRFérgica do núcleo leito da estria terminal nas alterações cardiovasculares induzidas pelo estresse: interação com a via de sinalização receptor NMDA / óxido nítrico/guanilato ciclase / proteína quinase g?
Beneficiário:Carlos Cesar Crestani
Modalidade de apoio: Auxílio à Pesquisa - Regular