Vasopressin deficiency diminishes acute and long-term consequences of maternal deprivation in male rat pups

D. Zelena, Berhard Stocker, I. Barna, Z. Tóth, G. Makara

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

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 24. h 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.

Original languageEnglish
Pages (from-to)378-391
Number of pages14
JournalPsychoneuroendocrinology
Volume51
DOIs
Publication statusPublished - Jan 1 2015

Fingerprint

Maternal Deprivation
Neurogenic Diabetes Insipidus
Vasopressins
Adrenocorticotropic Hormone
Weaning
Brattleboro Rats
Anniversaries and Special Events
Corticosterone
Mood Disorders
Weight Loss
Anxiety
Genotype
Body Weight

Keywords

  • ACTH
  • Corticosterone
  • CRH
  • Male Brattleboro pup
  • Stress-related behavior

ASJC Scopus subject areas

  • Endocrinology
  • Endocrinology, Diabetes and Metabolism
  • Psychiatry and Mental health
  • Biological Psychiatry
  • Endocrine and Autonomic Systems
  • Medicine(all)

Cite this

@article{745c4f913dc94d9fb332c7a207cea450,
title = "Vasopressin deficiency diminishes acute and long-term consequences of maternal deprivation in male rat pups",
abstract = "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 24. h 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.",
keywords = "ACTH, Corticosterone, CRH, Male Brattleboro pup, Stress-related behavior",
author = "D. Zelena and Berhard Stocker and I. Barna and Z. T{\'o}th and G. Makara",
year = "2015",
month = "1",
day = "1",
doi = "10.1016/j.psyneuen.2014.10.018",
language = "English",
volume = "51",
pages = "378--391",
journal = "Psychoneuroendocrinology",
issn = "0306-4530",
publisher = "Elsevier Limited",

}

TY - JOUR

T1 - Vasopressin deficiency diminishes acute and long-term consequences of maternal deprivation in male rat pups

AU - Zelena, D.

AU - Stocker, Berhard

AU - Barna, I.

AU - Tóth, Z.

AU - Makara, G.

PY - 2015/1/1

Y1 - 2015/1/1

N2 - 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 24. h 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.

AB - 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 24. h 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.

KW - ACTH

KW - Corticosterone

KW - CRH

KW - Male Brattleboro pup

KW - Stress-related behavior

UR - http://www.scopus.com/inward/record.url?scp=84920597530&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84920597530&partnerID=8YFLogxK

U2 - 10.1016/j.psyneuen.2014.10.018

DO - 10.1016/j.psyneuen.2014.10.018

M3 - Article

VL - 51

SP - 378

EP - 391

JO - Psychoneuroendocrinology

JF - Psychoneuroendocrinology

SN - 0306-4530

ER -