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This Article Full Text Full Text (PDF) All Versions of this Article: JOE-09-0096v1 202/2/263    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Zelena, D. Articles by Filaretova, L. PubMed PubMed Citation Articles by Zelena, D. Articles by Filaretova, L.

Institute of Experimental Medicine, Hungarian Academy of Science, PO Box 67, H-1450 Budapest, Hungary
¹ Department of Zoology and Biotechnology, Dr Harisingh Gour University, Sagar 470003 MP, India
² Department of Pyschiatry, University of Cincinnati, Cincinnati, Ohio 45237, USA
³ Pavlov Institute of Physiology, Russian Academy of Sciences, St Petersburg 199034, Russia

(Correspondence should be addressed to D Zelena; Email: zelena{at}koki.hu)

Adaptation to a constantly changing environment is fundamental to every living organism. The hypothalamic–pituitary–adrenocortical (HPA) axis is a key component of the adaptation process. The present study tests the hypothesis that vasopressin (AVP) is required for the HPA response to acute stimuli. To accomplish this, naturally AVP-deficient Brattleboro rats were exposed to a wide range of stimuli and their HPA response was compared with heterozygous littermattes. The circadian rhythmicity of plasma ACTH and corticosterone was not different between the two genotypes. The ACTH and corticosterone response to volume load, restraint or aggressive attack were decreased in AVP-deficient rats. The stress-induced increase in ACTH, but not corticosterone, was significantly impaired in AVP-deficient animals after novelty, elevated plus-maze, forced swim, hypoglycaemia, ulcerogenic cold immobilisation, lipopolysaccharide, hypertonic saline and egg white injection. The HPA response to social avoidance, ether inhalation and footshock was not different between the genotypes. In vitro, the hypophysis of AVP-deficient animals showed a reduction in stimulated ACTH production and their adrenal glands were hyporeactive to ACTH. A dissociation between the ACTH and corticosterone response was observed in several experiments and could not be explained by an earlier ACTH peak or enhanced adrenal sensitivity, suggesting the existence of paraadenohypophyseal neuroendocrine regulators. Loss of AVP affected the HPA response to a wide variety of stressors. Interestingly, the contribution of AVP to the HPA response was not specific for, nor limited to, a known stressor category. Thus, there is a context-specific requirement for AVP in stress-induced activation of the HPA axis.