Importance of the central nucleus of the amygdala on sodium intake caused by deactivation of lateral parabrachial nucleus

Autor(es)

Andrade-Franze, Glaucia M. F. ^[1] ; Andrade, Carina A. F. ^[1] ; Gasparini, Silvia ^[1] ; De Luca, Jr., Laurival A. ^[1] ; De Paula, Patricia M. ^[1] ; Colombari, Debora S. A. ^[1] ; Colombari, Eduardo ^[1] ; Menani, Jose V. ^[1]

Afiliação do(s) autor(es)

^[1] Sao Paulo State Univ UNESP, Sch Dent, Dept Physiol & Pathol, BR-14801903 Araraquara, SP - Brazil

• Tipo de documento: Artigo Científico
• Fonte: Brain Research; v. 1625, p. 238-245, NOV 2 2015.
• Citações Web of Science: 3

Resumo

The lateral parabrachial nucleus (LPBN) and the central nucleus of the amygdala (CeA) are important central areas for the control of sodium appetite. In the present study, we investigated the importance of the facilitatoxy mechanisms of the CeA on NaCl and water intake produced by the deactivation of LPBN inhibitory mechanisms. Male Holtzman rats (n=7-14) with stainless steel cannulas implanted bilaterally in the CeA and LPBN were used. Bilateral injections of moxonidine (alpha(2)-adrenoceptor/imidazoline agonist, 0.5 nmol/0.2 mu l) into the LPBN increased furosemide+captopril-induced 0.3 M NaCl (29.7 +/- 7.2, vs. vehicle: 4.4 +/- 1.6 ml/2 h) and water intake (26.4 +/- 6.7, vs. vehicle: 8.2 +/- 1.6 ml/2 h). The GABA(A) agonist muscimol (0.25 nmol/0.2 mu l) injected bilaterally into the CeA abolished the effects of moxonidine into the LPBN on 0.3 M NaCl (2.8 +/- 1.6 ml/2 h) and water intake (3.3 +/- 2.3 ml/2 h). Euhydrated rats treated with muscimol (0.5 nmol/0.2 mu l) into the LPBN also ingested 0.3 M NaCl (19.1 +/- 6.4 ml/4 h) and water (8.8 +/- 3.2 ml/4 h). Muscimol (0.5 nmol/0.2 mu l) into the CeA also abolished 0.3 M NaCl (0.1 + 0.04 ml/4 h) and water intake (0.1 +/- 0.02 ml/4 h) in euhydrated treated with muscimol into the LPBN. The present results show that neuronal deactivation of the CeA abolishes NaCl intake produced by the blockade of LPBN inhibitory mechanisms, suggesting an interaction between facilitatory mechanisms of the CeA and inhibitory mechanisms of the LPBN in the control of NaCl intake. (C) 2015 Elsevier B.V. All rights reserved. (AU)

• Processo FAPESP: 11/50770-1 - Mecanismos neurais de regulação do equilíbrio hidroeletrolítico e controle cardiorrespiratório
• Beneficiário: José Vanderlei Menani
• Modalidade de apoio: Auxílio à Pesquisa - Temático