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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.)

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

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Author(s):
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]
Total Authors: 8
Affiliation:
[1] Sao Paulo State Univ UNESP, Sch Dent, Dept Physiol & Pathol, BR-14801903 Araraquara, SP - Brazil
Total Affiliations: 1
Document type: Journal article
Source: Brain Research; v. 1625, p. 238-245, NOV 2 2015.
Web of Science Citations: 3
Abstract

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)

FAPESP's process: 11/50770-1 - Neural mechanisms involved of hydroelectrolytic balance and cardiorespiratory control
Grantee:José Vanderlei Menani
Support Opportunities: Research Projects - Thematic Grants