Intersections of sex and corticotropin-releasing factor

摘要

Since its original identification and characterization in 1981 by Vale et al. (1), corticotropin-releasing factor (CRF)—now also called corticotropin-releasing hormone—has been intimately linked with stress regulation and conditioned fear and anxiety. For example, knockout of the CRF receptor 1 (CRFri) has anxiolytic effects (2,3), while CRF overexpression increases conditioned fear (4). With the increasing availability of highly selective tools, roles for CRF in discrete cell populations have also been established. For example, Gafford et al. (5) selectively knocked down gamma-aminobutyric acid (GABA) Aa1 receptor subunits in CRF-containing cells within the amygdala. This procedure impaired fear extinction; in other words, mice with this highly selective deficiency are incapable of learning that a previously shock-associated cue is no longer threatening, implicating CRF systems in pathologies such as posttraumatic stress disorder.