Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Maternal separation (MS) has been used to model the causal relationship between early life stress and the later stress-over-reactivity and affective disorders. Arginine vasopressin (AVP) is among several factors reported to be abnormal. The role of AVP on anxiety is still unclear. In order to further investigate this causal relationship and its possible role in anxiogenesis, male rat pups were separated from their dams for 3h daily (3 hMS) from post-natal day (PND) 2 to PND15. Fos expression in AVP+ neurons in the hypothalamic paraventricular (PVN) and supraoptic nuclei (SON) triggered by 3 hMS, and AVP-mRNA expression, were examined at PND10 and PND21 respectively, whereas AVP-mRNA expression, PVN and SON volumes and plasma AVP concentration were assessed in adulthood. Elevated plus maze test (EPM) and Vogel conflict test (VCT) were also performed to evaluate unconditioned and conditioned anxious states at PND70-75. At PND10, a single 3hMS event increased Fos expression in AVP+ neurons fourfold in PVN and six to twelvefold in SON. AVP-mRNA was over-expressed in whole hypothalamus, PVN and SON between 122% and 147% at PND21 and PND63. Volumes of AVP-PVN and AVP-SON measured at PND75 had marked increases as well as AVP plasma concentration at 12h of water deprivation (WD). MS rats demonstrated a high conditioned anxious state under VCT paradigm whereas no difference was found under EPM. These data demonstrate direct relationships between enhanced AVP neuronal activation and a potentiated vasopressin system, and this latter one with high conditioned anxiety in MS male rats.
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PMID:Hypothalamic vasopressin system regulation by maternal separation: its impact on anxiety in rats. 2252 66

Early life events have special importance in the development as postnatal environmental alterations may permanently affect the lifetime vulnerability to diseases. For the interpretation of the long-term consequences it is important to understand the immediate effects. As the role of vasopressin in hypothalamic-pituitary-adrenal axis regulation as well as in affective disorders seem to be important we addressed the question whether the congenital lack of vasopressin will modify the stress reactivity of the pups and will influence the later consequences of single 24h maternal deprivation (MD) on both stress-reactivity and stress-related behavioral changes. Vasopressin-producing (di/+) and deficient (di/di) Brattleboro rat were used. In 10-day-old pups MD induced a remarkable corticosterone rise in both genotypes without adrenocorticotropin (ACTH) increase in di/di rats. Studying the later consequences at around weaning (25-35-day-old rats) we found somatic and hormonal alterations (body weight reduction, dysregulation of the stress axis) which were not that obvious in di/di rats. The more anxious state of MD rats was not detectable in di/di rats both at weaning and in adulthood (7-12-week-old). The lack of vasopressin abolished all chronic stress and anxiety-like tendencies both at weaning and in adulthood probably as a consequence of reduced ACTH rise immediately after MD in pups. This finding suggests that postnatal stress-induced ACTH rise may have long-term developmental consequences.
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PMID:Vasopressin deficiency diminishes acute and long-term consequences of maternal deprivation in male rat pups. 2546 10