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Modulation of CRH and AVP as a therapeutic strategy in anxiety disorders
The neuroendocrine and behavioral phenotypes of depression and anxiety disorders are at least in part mediated via modulation of corticotropin-releasing hormone (CRH) and vasopressin (AVP) neurocircuitry and normalization of an altered neurotransmission after treatment may lead to restoration of disease-related alterations. The CRH1 receptor antagonist R121919 and paroxetine were tested in rats selectively bred for high (HAB) trait anxiety. The high emotionality of HAB rats is accompanied by an aberrant outcome of the DEX/CRH test, which could be shown to be related to a hypothalamic AVP hyperdrive. The findings provide first direct evidence that modulation of the vasopressinergic and CRH systems is likely to be critically involved in the behavioral and neuroendocrine effects of anxiolytic and antidepressant drugs. Work in progress focuses on HPA-system associated genes in patients.
Supported by DFG