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. Author manuscript; available in PMC: 2007 Jul 1.
Published in final edited form as: J Neuroendocrinol. 2007 Jul;19(7):543–551. doi: 10.1111/j.1365-2826.2007.01560.x

Figure 2.

Figure 2

HPA axis activity in male Avpr1b KO and wild-type mice 30 min after administration of EtOH (3.2g/kg i.p.). Values are mean ± SEM, n = 4-5 mice/group. A = ACTH; B = CORT. a, P < 0.001 EtOH wild-type vs. vehicle (veh) wild-type; b, P < 0.01 EtOH wild-type vs. EtOH KO; c, P < 0.05 EtOH KO vs. vehicle KO. There is no significant difference (P > 0.05) between vehicle wild-type and vehicle KO plasma ACTH or CORT levels. There is also no significant difference between handled and saline plasma ACTH and CORT levels in either genotype (e.g., plasma ACTH levels: 18.3 ± 8.3 and 23.7 ± 6.0 pg/ml for handled and saline-treated KO mice, respectively, and 24.4 ± 7.3 and 17.5 ± 3.4 pg/ml for handled and saline-treated wild-type mice, respectively; mean ± SEM, n = 4-5). Blood alcohol measurements (BALs) are shown in (C). a, P < 0.0001 EtOH vs. vehicle; ND, not detectable. There is no significant difference between EtOH wild-type and EtOH KO plasma BALs.