Adrenergic and glutamatergic mechanisms of the lateral parabrachial nucleus in the control of sodium appetite

• Grant number: 13/20909-3
• Support Opportunities: Scholarships in Brazil - Scientific Initiation
• Start date: December 01, 2013
• End date: November 30, 2015
• Field of knowledge: Biological Sciences - Physiology - Physiology of Organs and Systems
• Principal Investigator: Carina Aparecida Fabrício de Andrade
• Grantee: Camilla Dias Guillen
• Host Institution: Faculdade de Odontologia (FOAr). Universidade Estadual Paulista (UNESP). Campus de Araraquara. Araraquara , SP, Brazil

Abstract

Different neurotransmitters and receptors present in the lateral parabrachial nucleus (LPBN) affect the activity of inhibitory mechanisms of this area. Serotonin, cholecystokinin, corticotropin releasing factor and glutamate act in the LPBN activating inhibitory mechanisms and reducing sodium intake and occasionally water intake. On the other hand, activation of ±2-adrenergic receptors, opioid, GABAergic, purinergic receptors reduces the activity of inhibitory mechanisms thus increasing sodium intake. It has been shown that of ±2-adrenergic receptor activation in the LPBN may release GABA and opioids, and additionally promote a blockade of serotonin action in this area. The results from our previous study show that LPBN injection of PPADS (2 nmol) reduced the potent increase in 0.3 M NaCl and water the intake induced by moxonidine (0.5 nmol) injection. These data suggest that there is an interaction between purinergic and adrenergic mechanisms in the LPBN to control acute sodium appetite. However, the hypothesis of interaction between ±2-adrenergic receptors and other LPBN neurotransmitter/mechanisms that act in the LPBN activating inhibitory mechanisms (e.g., glutamate) has not been tested yet. In order to study a possible interaction between adrenergic and glutamate receptors in the LPBN, Holtzman rats with bilateral stainless steel cannula implanted into the LPBN will be used. Sodium and water intake will be studied in rats submitted to an acute model of sodium appetite (treatment with diuretics furosemide associated with angiotensin converting enzyme inhibitor captopril), which will receive different combinations of glutamate and ±2-adrenergic receptors antagonists and agonists into the LPBN.