CRF2 null mutation increases sensitivity to isolation rearing effects on locomotor activity in mice

摘要

BackgroundDevelopmental stressors are consistently reported to increase risk for certain neuropsychiatric disorders including schizophrenia, depression, and post-traumatic stress disorder. Recent clinical evidence supports a “double-hit” hypothesis of genetic vulnerability interacting with developmental challenges to modulate this risk. Early life stressor effects on behavior may be modulated in part by alterations in corticotropin releasing factor (CRF) signaling via two known receptors, CRF1 and CRF2. One extant hypothesis is that CRF2 activation may modulate long term adaptive responses after homeostatic challenge. As such, loss of CRF2 activity via genetic variance may increase sensitivity to the long-term effects of developmental stress.