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. 2019 Apr 24;317(2):R289–R300. doi: 10.1152/ajpregu.00029.2019

Fig. 1.

Fig. 1.

Acyloxyacyl hydrolase (AOAH)-deficient mice exhibit depressive-like behavioral phenotypes and corticotropin-releasing factor (Crf) dysregulation. A: female AOAH-deficient mice exhibit increased latency to reach food in novelty suppressed feeding assay (n = 17–18, P = 0.0006, two-tailed Student’s t-test). B: female AOAH-deficient mice consume food pellet (P = 0.0060), compared with wild-type (WT) mice. C: female Aoah−/− mice showed decreased preference for sucrose water in sucrose preference test as compared with B6 mice (n = 10–12, P = 0.0016, two-tailed Student’s t-test,). D: quantitation of Crf mRNA of WT and AOAH-deficient brain punches from the paraventricular nucleus (PVN) normalized to ribosomal protein L19. Female Aoah−/− mice have increased PVN Crf mRNA (n = 14–19, P = 0.0109, two-tailed Student’s t-test). E: female Aoah−/− mice have increased serum corticosterone by ELISA (n = 14–16, P = 0.0148, Mann-Whitney U-test). Data are means ± SE. Differences were considered statistically significant at *P < 0.05; **P < 0.01; ***P < 0.001.