These translational data suggest that genetic variation in CRHR1 affects the risk for affective disorders by influencing the function of the neural circuit underlying AT and that differences in gene expression or the protein sequence involving exon 6 may be important.
Our results suggest possible involvement of the AVPR1b and CRHR1 genes in the ethiology of psychotic features in the course of affective disorders, and possible involvement of CRHR1 gene in the ethiology of bipolar disorder.
Deficient beta-arrestin-2-CRF(1) receptor interactions could contribute to the pathophysiology of affective disorders by inducing excessive CRF(1) receptor signaling.