, 1984, Fulwiler and Saper, 1984, Herbert et al., 1990, Jhamandas et al., 1992, Jhamandas

et al., 1996 and Norgren, 1981). Therefore, the LPBN may convey signals that ascend from AP/mNTS to the forebrain areas that regulate fluid and electrolyte balance and related behaviors like water and sodium intake. Numerous neurotransmitter systems have implicated the LPBN in the control of sodium intake. For example, bilateral LPBN injections of methysergide, a serotonergic receptor antagonist, increase hypertonic NaCl intake induced by angiotensin II (ANG II) administered intracerebroventricularly (i.c.v.) or into the subfornical organ Selisistat research buy (SFO), by 24 h of water deprivation, by 24 h of sodium depletion or by deoxycorticosterone acetate (DOCA) (De Gobbi et al., 2001, Menani et al., 1996, Menani et al., 1998a, Menani et al., 2000 and Menani and Johnson, 1995). Blockade of cholecystokinin (CCK) or serotonin receptors or activation of α2-adrenergic receptors in the LPBN enhances NaCl intake by rats injected subcutaneously

with the diuretic furosemide (FURO) combined with the angiotensin converting enzyme inhibitor captopril (CAP) (Andrade et al., 2004, De Gobbi et al., 2001, Menani et al., 1996 and Menani et al., 1998b). The blockade of LPBN neurons with bilateral injections of the GABAA agonist muscimol induces PCI-32765 order robust ingestion of hypertonic NaCl and slight ingestion of water in fluid replete rats and increases FURO + CAP- and 24 h sodium depletion-induced sodium intake, suggesting that a GABAergic

mechanism present in LPBN is involved in the control of sodium intake (Callera et al., 2005 and De Oliveira et al., 2007). The cardiovascular, neuroendocrine and ingestive effects of ANG II acting centrally are mediated mainly by angiotensin type 1 (AT1) receptors located in different areas of the central nervous system, such as the LPBN, anterior hypothalamic area (AHA), amygdala, SFO, rostral and caudal ventrolateral medulla and NTS (Fitzsimons, 1998, Fregly and Rowland, 1991, Mckinley et al., 1996, Rowland et al., 1992 and Thunhorst and Fitts, 1994). The nonpeptide antagonist losartan selectively binds on AT1 receptors (Chiu et al., 1989). Studies using whole cell voltage-clamp Megestrol Acetate techniques have suggested that ANG II acting on AT1 receptors may modulate GABAergic synaptic transmission and produce opposite effects, depending on whether pre- or post-synaptic AT1 receptors are activated (Henry et al., 2009, Li et al., 2003, Li and Pan, 2005 and Xing et al., 2009). It has been suggested that ANG II acting on pre-synaptic AT1 receptors reduces GABA release and decreases the amplitude of evoked GABAergic inhibitory post-synaptic currents (IPSCs) (Li et al., 2003, Li and Pan, 2005 and Xing et al., 2009). In contrast, it was shown that endogenous ANG II acting on post-synaptic AT1 receptors increases IPSCs in sodium-sensitive neurons in the median preoptic nucleus (MnPO) (Henry et al., 2009).