Hypothalamic CRH and vasopressin expression in animal models of depression and anxiety
Hypersecretion of the hypothalamic corticotropin-releasing hormone (CRH), the main neuroendocrine hypothalamic-pituitaryadrenal (HPA) axis stimulator, is supposed to be the reason of HPA axis abnormalities observed in depression and anxiety. It was also suggested that vasopressin as the major CRH secretagogue might be involved in HPA axis hyperactivity described in depression. But neuroendocrine mechanisms of depression and anxiety are still not revealed. The aim of the present study was to elucidate the role of hypothalamic CRH- and vasopressin-producing centres in the development of depressive- and anxiety-like states in rats. Animal models have been applied, including the “learned helplessness” as a model of depression and Time-dependent sensitization paradigm as a model of anxiety disorder (posttraumatic stress disorder, PTSD, in particular). The depressive- and anxiety-like states in rats are characterized by signifi cant increase of CRH-immunoreactivity in the parvocellular division of the paraventricular nucleus (PVN). Overexpression of CRH in the magnocellular PVN is involved in the development of anxiety- but not depressive-like state. Anxiety-like state in rats is accompanied by increase of vasopressin expression in the magnocellular part of the PVN, suggesting its implication in the pathogenesis of PTSD. Our data give evidence of common and specifi c mechanisms of depression and anxiety and might be useful in working out new approaches in treatment of these disorders.