Both N-methyl-D-aspartate and non-N-methyl-D-aspartate glutamate receptors in the bed nucleus of the stria terminalis modulate the cardiovascular responses to acute restraint stress in rats

• Autor(a) principal: Adami, Mariane B. [UNESP]
• Data de Publicação: 2017
• Outros Autores: Barretto-De-Souza, Lucas [UNESP], Duarte, Josiane O. [UNESP], Almeida, Jeferson [UNESP], Crestani, Carlos C. [UNESP]
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Repositório Institucional da UNESP
• Texto Completo: http://dx.doi.org/10.1177/0269881117691468; http://hdl.handle.net/11449/174717
• topic: arterial pressure; autonomic activity; Bed nucleus of the stria terminalis; extended amygdala; heart rate; sympathetic activity

The bed nucleus of the stria terminalis (BNST) is a forebrain structure that has been implicated on cardiovascular responses evoked by emotional stress. However, the local neurochemical mechanisms mediating the BNST control of stress responses are not fully described. In our study we investigated the involvement of glutamatergic neurotransmission within the BNST in cardiovascular changes evoked by acute restraint stress in rats. For this study, we investigated the effects of bilateral microinjections of selective antagonists of either N-methyl-D-aspartate (NMDA) or non-NMDA glutamate receptors into the BNST on the arterial pressure and heart rate increase and the decrease in tail skin temperature induced by acute restraint stress. Microinjection of the selective NMDA glutamate receptor antagonist LY235959 (1 nmol/100 nL) into the BNST decreased the tachycardiac response to restraint stress, without affecting the arterial pressure increase and the drop in skin temperature. Bilateral BNST treatment with the selective non-NMDA glutamate receptor NBQX (1 nmol/100 nL) decreased the heart rate increase and the fall in tail skin temperature, without affecting the blood pressure increase. These findings indicate a facilitatory influence of BNST glutamatergic neurotransmission via coactivation of local NMDA and non-NMDA receptors on the tachycardiac response to stress, whereas control of sympathetic-mediated cutaneous vasoconstriction is selectively mediated by local non-NMDA glutamate receptors.