5, P > 0 05) or HR (353 ± 11 vs 372 ± 6 bpm, t = 1 6, P > 0 05)

5, P > 0.05) or HR (353 ± 11 vs. 372 ± 6 bpm, t = 1.6, P > 0.05) baseline values. Pretreatment of the contralateral SON with aCSF also did not affect both the pressor (44 ± 4

vs. 37 ± 3 mm Hg, t = 2.2, P > 0.05) and bradycardiac (− 67 ± 8 vs. − 74 ± 8 bpm, t = 0.5, P > 0.05) response to carbachol microinjection into the BST ( Fig. 1A). Microinjection of CoCl2 into the contralateral Ipilimumab order SON (n = 6) did not affect either MAP (101 ± 3 vs. 100 ± 4 mm Hg, t = 0.1, P > 0.05) or HR (362 ± 9 vs. 359 ± 10 bpm, t = 0.3, P > 0.05) baseline values. However, contralateral SON pretreatment with CoCl2 significantly reduced the pressor (42 ± 5 vs. 9 ± 2 mm Hg, t = 5, P < 0.005) and bradycardiac (− 74 ± 6 vs. − 13 ± 2 bpm, t = 10, P < 0.0001) response to carbachol microinjection into the BST ( Fig. 1A). Time-course analysis indicated a significant

effect of SON pretreatment with CoCl2 in carbachol cardiovascular effects (ΔMAP: F(1,380) = 215, P < 0.0001 and ΔHR: F(1,380) = 141, P < 0.0001), a significant effect over time (ΔMAP: F(37,380) = 16, P < 0.0001 and ΔHR: F(37,380) = 8, P < 0.0001), and an interaction between treatment and time (ΔMAP: F(37,380) = 11, P < 0.0001 and ΔHR: F(37,380) = 3, P < 0.0001) ( Fig. 1B). Cardiovascular responses to carbachol microinjection into the BST of animals that received CoCl2 in the ipsilateral or contralateral SON were not significantly different (MAP: t = 2, P > 0.05; HR: t = 1, P > 0.05) ( Fig. 1). Representative Alectinib in vitro recordings showing the cardiovascular responses to carbachol microinjection into the BST before and after ipsilateral or contralateral SON pretreatment with CoCl2 is presented in Fig. 3. Moreover, photomicrography of coronal brain section showing the microinjection site in the ipsilateral and contralateral SON of representative animals are presented in Fig. 4 and Fig. 5, respectively. Diagrammatic representation

showing microinjection sites of CoCl2 and aCSF in the ipsilateral and contralateral SON is also shown in Fig. 4 and Fig. 5, respectively. Microinjection of aCSF into the ipsilateral PVN (n = 7) did not affect either MAP (99 ± 3 vs. 102 ± 2 mm Hg, t = 0.6, P > 0.05) or HR (357 ± 7 vs. 364 ± 10 bpm, t = 0.5, P > 0.05) baseline values. Ipsilateral PVN treatment with aCSF also did not affect the pressor (43 ± 3 vs. 40 ± 2 mm Hg, t = 0.7, P > 0.05) the and bradycardiac (− 78 ± 6 vs. − 73 ± 5 bpm, t = 0.8, P > 0.05) response following carbachol microinjection into the BST ( Fig. 6A). Microinjection of CoCl2 into the ipsilateral PVN (n = 7) did not affect either MAP (99 ± 3 vs. 100 ± 3 mm Hg, t = 0.8, P > 0.05) or HR (366 ± 9 vs. 374 ± 9 bpm, t = 0.5, P > 0.05) baseline values. Moreover, ipsilateral PVN pretreatment with CoCl2 did not affect the pressor (41 ± 3 vs. 38 ± 2 mm Hg, t = 0.9, P > 0.05) and bradycardiac (− 76 ± 8 vs. − 73 ± 6 bpm, t = 0.3, P > 0.05) response to carbachol microinjection into the BST ( Fig. 6A).

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