The neuropeptide arginine vasopressin (AVP) is released within distinct brain areas upon appropriate stimulation, including stressful challenges. Following its predominantly dendritic release, AVP triggers a variety of receptor-mediated effects related to behavioral and neuroendocrine regulation. Antagonist treatment together with other sophisticated loss-of-function and gain-of-function approaches provide evidence for a multiple involvement of V1a and V1b receptor subtypes in stress-related behavior and disorders, including anxiety disorders, comorbid depression and their neuroendocrine concomitants. Conversely, in the high versus low anxiety (HAB/LAB) rat model, the phenotype of extreme trait anxiety is associated with a polymorphism-driven overexpression of AVP in the hypothalamic paraventricular nucleus. This overexpression of AVP might be considered a final common pathway of anxiety-related behavior. The capability of both responding to stressful stimuli and mediating genetic polymorphisms makes the central release of AVP a key process for converging (i.e., environmentally and genetically driven) behavioral regulation. Polymorphisms in the promoter structures of the AVP gene and AVP receptor genes, underlying differences in gene expression, thus contribute to individual variation in behavior as well as to psychopathology, making genes of the brain AVP system and their products a promising target for therapeutic interventions.
Keywords: receptor, antagonist, stress, emotionality, HAB, social behavior, depression, anxiety, AVP, Vasopressin
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