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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 1.

Figure 1

Effect of LPS on HPA axis activity in female Avpr1b KO and wild-type mice. Animals were sacrificed 30min following LPS (100μg i.p.) or saline challenge, and plasma levels of ACTH (A) and CORT (B) were measured. Values are mean ± SEM, n = 5-6 mice/treatment group. a, P < 0.0001 LPS wild-type vs. LPS KO; b, P < 0.001 LPS wild-type vs. saline wild-type; c, P < 0.05 LPS KO vs. saline KO. There is no significant difference (P > 0.05) between saline wild-type and saline KO plasma ACTH or CORT levels. There is also no significant difference between handled (mice briefly handled and returned to home cage 30min prior to sacrifice) and saline plasma ACTH and CORT levels in either genotype (e.g., plasma ACTH levels: 17.8 ± 4.9 and 20.4 ± 3.3 pg/ml for handled and saline-treated KO mice, respectively, and 22.4 ± 8.2 and 22.3 ± 4.5 pg/ml for handled and saline-treated wild-type mice, respectively; mean ± SEM, n = 4-5). In (C) plasma CORT levels were measured 4 h after LPS or saline challenge. Values are mean ± SEM, n = 3-4 animals/group. a, P < 0.0001 LPS vs. saline. There is no significant difference (P > 0.05) between saline- or LPS-stimulated CORT levels for both genotypes.