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Neuroscience. 2015 Jan 22;284:768-74. doi: 10.1016/j.neuroscience.2014.09.042. Epub 2014 Sep 28.

Moxonidine into the lateral parabrachial nucleus modifies postingestive signals involved in sodium intake control.

Author information

1
Department of Physiology and Pathology, School of Dentistry, São Paulo State University (UNESP), Araraquara, Brazil.
2
Department of Physiology and Pathology, School of Dentistry, São Paulo State University (UNESP), Araraquara, Brazil. Electronic address: menani@foar.unesp.br.
3
Department of Psychology, University at Buffalo, The State University of New York, United States.

Abstract

The activation of α2-adrenoceptors with bilateral injections of moxonidine (α2-adrenoceptor and imidazoline receptor agonist) into the lateral parabrachial nucleus (LPBN) increases 1.8% NaCl intake induced by treatment with furosemide (FURO)+captopril (CAP) subcutaneously. In the present study, we analyzed licking microstructure during water and 1.8% NaCl intake to investigate the changes in orosensory and postingestive signals produced by moxonidine injected into the LPBN. Male Sprague-Dawley rats were treated with FURO+CAP combined with bilateral injections of vehicle or moxonidine (0.5 nmol/0.2 μl) into the LPBN. Bilateral injections of moxonidine into the LPBN increased FURO+CAP-induced 1.8% NaCl intake, without changing water intake. Microstructural analysis of licking behavior found that this increase in NaCl intake was a function of increased number of licking bursts from 15 to 75 min of the test (maximum of 49±9 bursts/bin, vs. vehicle: 2±2 bursts/bin). Analysis of the first 15 min of the test, when most of the licking behavior occurred, found no effect of moxonidine on the number of licks/burst for sodium intake (24±5 licks/burst, vs. vehicle: 27±8 licks/burst). This finding suggests that activation of α2-adrenoceptors in the LPBN affects postingestive signals that are important to inhibit and limit sodium intake by FURO+CAP-treated rats.

KEYWORDS:

parabrachial nucleus; postingestive; sodium intake; α(2)-adrenoreceptors

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