期刊论文详细信息
PSYCHONEUROENDOCRINOLOGY 卷:51
Vasopressin deficiency diminishes acute and long-term consequences of maternal deprivation in male rat pups
Article
Zelena, Dora1  Stocker, Berhard1  Barna, Istvan1  Toth, Zsuzsanna E.2  Makara, Gabor B.1 
[1] Hungarian Acad Sci, Inst Expt Med, Budapest, Hungary
[2] Semmelweis Univ, Dept Anat Histol & Embryol, H-1085 Budapest, Hungary
关键词: Male Brattleboro pup;    CRH;    ACTH;    Corticosterone;    Stress-related behavior;   
DOI  :  10.1016/j.psyneuen.2014.10.018
来源: Elsevier
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【 摘 要 】

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. (C) 2014 Elsevier Ltd. All rights reserved.

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