Intact acyl-ghrelin signaling via GHSRs minimizes CSDS-associated, depression-like behavior.
CSDS induces depression-like behaviors, as indicated by (A) decreased time subjects spend in the interaction zone near the target mouse and (B) increased time subjects spend in the corners of the social interaction test arena, as compared with that of non-CSDS-exposed mice (n = 20 per group). GHSR deletion aggravates these behaviors (*P < 0.05, **P = 0.0012). (C) CSDS increases plasma acyl-ghrelin (D) but not desacyl-ghrelin, in wild-type and GHSR-null mice (n = 6–7 per group). (E) CSDS increases plasma corticosterone, but this effect is not as pronounced in GHSR-null mice (*P < 0.05; n = 15–18 per group). Significant effects of treatment (CSDS vs. control non-CSDS) and significant genotype X treatment interactions are indicated.