In the present study, we show results indicating that carbachol microinjection into the BST increases circulating vasopressin levels, thus confirming previous evidence that carbachol microinjection into the BST evokes pressor response due to vasopressin release. Vasopressin is a potent vasoconstrictor agent (Altura and Altura, 1984 and Barer, 1961). This nonapeptide is synthesized by magnocellular neurons of the PVN and SON (Swaab et al., 1975). Each neuron gives rise to a single axon into the posterior pituitary gland, where its neurosecretory endings release vasopressin

(Swaab et al., 1975). Because the capillaries within the pituitary gland do not have a blood-brain barrier, vasopressin released in close proximity to the capillaries easily enters p38 MAPK signaling the bloodstream (Leng et al., 1999). To verify if SON and/or PVN synapses mediate the pressor response to the carbachol microinjection into the BST, we pretreated both nuclei with the nonselective neurotransmission blocker CoCl2. The use of CoCl2 is a common approach to investigate a possible involvement of specific brain areas in a functional neural pathway. The technique is based on the administration of circumscribed microinjections of compounds that reversibly

block neuronal activity over a given period of time. The microinjection of CoCl2 into discrete brain areas has been used for the functional inactivation of synapses (Crestani et al., 2006, Crestani et al., 2009b, Giancola et al., 1993 and Scopinho et al., 2008). The CoCl2 reduces presynaptic Ca+ 2 influx, leading to an Selleckchem Doxorubicin inhibition of neurotransmitter release and a consequent synaptic blockade (Kretz, 1984), without influence

on passage fibers. The inhibition caused by this compound, when Inositol monophosphatase 1 microinjected in volumes and concentrations that were similar to those presently used, was reported to spread over an area up to 1 mm2 (Lomber, 1999). Pretreatment of the PVN with CoCl2, either injected ipsilateral or contralateral in relation to BST microinjection site, did not affect the cardiovascular response to the microinjection carbachol into the BST. The absence of effect was not due to an insufficient dose of CoCl2, because in previous studies it has been reported that the microinjection of such dose into the PVN was effective to inhibit vasopressin-mediated pressor responses observed after the injection of noradrenaline into either the BST or the lateral septal area (Crestani et al., 2009b and Scopinho et al., 2008). Pretreatment of either the ipsilateral or the contralateral SON with CoCl2 blocked the pressor and bradycardiac responses caused by the microinjection carbachol into the BST. Together, these results suggest that synapses in the SON, but not in the PVN, mediate the cardiovascular responses to the microinjection of carbachol into the BST.