05; ΔHR: F(1,456) = 2, PD0325901 price P > 0.05), but indicated a significant effect over

time on the MAP (F(37,456) = 45, P < 0.0001) and HR (F(37,456) = 18, P < 0.0001) ( Fig. 6B). Microinjection of aCSF into the contralateral PVN (n = 6) did not affect either MAP (101 ± 3 vs. 98 ± 2 mm Hg, t = 0.5, P > 0.05) or HR (353 ± 11 vs. 361 ± 7 bpm, t = 0.5, P > 0.05) baseline values. Contralateral PVN treatment with aCSF also did not affect the pressor (43 ± 4 vs. 39 ± 3 mm Hg, t = 0.8, P > 0.05) and bradycardiac (− 76 ± 9 vs. − 68 ± 6 bpm, t = 0.8, P > 0.05) response to carbachol microinjection into the BST ( Fig. 6A). Microinjection of CoCl2 into the contralateral PVN (n = 6) did not affect either MAP (99 ± 3 vs. 104 ± 4 mm Hg, t = 1.5, P > 0.05) or HR (359 ± 9 vs. 372 ± 12 bpm, t = 0.9, P > 0.05) baseline

values. Moreover, contralateral PVN pretreatment with CoCl2 did not affect the pressor (42 ± 4 vs. 41 ± 2 mm Hg, t = 0.1, P > 0.05) and bradycardiac (− 70 ± 9 vs. − 65 ± 8 bpm, t = 0.5, P > 0.05) response to carbachol microinjection into the BST ( Fig. 6A). Time-course analysis did not show a significant effect of contralateral PVN pretreatment with CoCl2 in carbachol cardiovascular responses (ΔMAP: F(1,380) = 2, P > 0.05; ΔHR: F(1,380) = 0.2, P > 0.05) ( Fig. 6B), but indicated a significant Wnt inhibitor effect over time on the MAP (F(37,380) = 44, P < 0.0001) and HR (F(37,380) = 11, P < 0.0001). Photomicrography of coronal brain section showing the microinjection site in the ipsilateral and contralateral PVN of representative animals is presented in Fig. 7 and Fig. 8, respectively. Diagrammatic representation showing microinjection sites of CoCl2

and aCSF in the ipsilateral and contralateral PVN is also shown in Fig. 7 and Fig. 8, respectively. The BST is localized in the rostral prosencephalon, and is associated with autonomic and neuroendocrine functions (Dunn, Celecoxib 1987, Dunn and Williams, 1995 and Ulrich-Lai and Herman, 2009). Cholinergic synaptic terminals were indentified in the BST (Ruggiero et al., 1990). Moreover, binding studies described the presence of muscarinic and nicotinic receptors in the BST (Clarke et al., 1985 and Wamsley et al., 1984). Electrophysiological studies reported that BST neurons showed an increase in firing rate in response to local administration of acetylcholine through activation of local muscarinic cholinergic receptors (Casada and Dafny, 1993a and Casada and Dafny, 1993b). We have previously reported that microinjection of carbachol, a cholinergic agonist, into the BST of unanesthetized rats evoked a pressor response that was followed by a baroreflex-mediated bradycardia (Alves et al., 2007). These cardiovascular effects were blocked after local pretreatment with an M2-muscarinic receptor antagonist as well as after systemic pretreatment with a V1-vasopressinergic receptor antagonist (Alves et al.