Interaction between facilitatory mechanisms and lateral parabrachial nucleus mechanisms in the control of sodium intake and oxytocin secretion

• Grant number: 10/20407-0
• Support Opportunities: Scholarships in Brazil - Doctorate
• Start date: December 01, 2012
• End date: August 31, 2014
• Field of knowledge: Biological Sciences - Physiology - Physiology of Organs and Systems
• Principal Investigator: José Vanderlei Menani
• Grantee: Camila Ferreira Roncari
• Host Institution: Faculdade de Odontologia (FOAr). Universidade Estadual Paulista (UNESP). Campus de Araraquara. Araraquara , SP, Brazil
• Associated research grant: 11/50770-1 - Neural mechanisms involved of hydroelectrolytic balance and cardiorespiratory control, AP.TEM

Abstract

Thirst and sodium appetite are regulated by central facilitatory mechanisms (activated by angiotensin II, mineralocorticoid or hyperosmolarity) and by central inhibitory mechanisms such as oxytocinergic and lateral parabrachial nucleus (LPBN) mechanisms. Injections of the GABAA agonist muscimol into the LPBN of normohydrated rats induce an intense sodium intake that is reduced by the blockade of AT1 angiotensinergic or central muscarinic receptors, indicating the importance of these facilitatory mechanisms for sodium intake in this condition. However, considering that the rats are normohydrated, these facilitatory mechanisms should not be activated, except if LPBN muscimol injections might activate these mechanisms. Or this effect might also be due to basaline central cholinergic or angiotensinergic activity. Therefore, the proposal is to investigate whether muscimol injection into the LPBN might activate the renin-angiotensin system. Moreover, we also propose to analyze the expression of c-fos in order to investigate which brain areas are activated after injections of muscimol into the LPBN. Contrary to the old concepts, it was recently shown that hyperosmolarity, as well as the central cholinergic activation may also facilitate sodium intake when the activity of LPBN inhibitory mechanisms is reduced. Hyperosmolarity and central cholinergic stimulation activate central oxytocinergic mechanisms which are inhibitory for sodium intake. Thus, another issue to be studied is whether the LPBN is involved with the control of oxytocinergic mechanisms. It would also be important to investigate where would be located the osmoreceptors that facilitate sodium intake. In this case, the proposal is to investigate whether neuronal deactivation of an area rich in osmoreceptors like the subfornical organ would affect sodium intake in hyperosmotic rats when the LPBN is blocked. (AU)

Scientific publications

(References retrieved automatically from Web of Science and SciELO through information on FAPESP grants and their corresponding numbers as mentioned in the publications by the authors)

DAVID, RICHARD B.; RONCARI, CAMILA F.; LAUAR, MARIANA R.; VENDRAMINI, REGINA C.; ANTUNES-RODRIGUES, JOSE; MENANI, JOSE V.; DE LUCA, JR., LAURIVAL A.. Sodium intake, brain c-Fos protein and gastric emptying in cell-dehydrated rats treated with methysergide into the lateral parabrachial nucleus. Physiology & Behavior, v. 151, p. 111-120, NOV 1 2015. (11/50770-1, 10/20407-0, 13/05189-4)