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The arginine vasopressin and corticotrophin‐releasing hormone gene transcription responses to varied frequencies of repeated stress in rats
Author(s) -
Ma XinMing,
Lightman Stafford L.
Publication year - 1998
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1111/j.1469-7793.1998.605bk.x
Subject(s) - habituation , vasopressin , endocrinology , medicine , corticosterone , stressor , arginine , corticotropin releasing hormone , hormone , neuropeptide , adrenocorticotropic hormone , glucocorticoid , gene expression , biology , neuroscience , gene , amino acid , biochemistry , receptor
1 Rats habituate to repeated exposure to homotypic stressors. The present studies were designed to define how altered frequency of exposure to a stressor affects the development of habituation and how this habituation is reflected in alterations in basal expression and responsiveness of hypothalamic corticotrophin‐releasing hormone (CRH) and arginine vasopressin (AVP) messenger and heteronuclear RNA (hnRNA). 2 Rats were exposed to a 60 min period of restraint stress every 7th day, every 3rd day, alternate days or daily for 2 weeks and their response to a final episode of stress on day 15 was compared with that of a control group of unstressed rats. 3 The response of plasma corticosterone to the final stressor on day 15 was diminished in animals which had been stressed on only two previous occasions, 7 days apart, and diminished further with increasing frequency of previous stressors until it failed to respond at all in animals stressed daily. 4 The pattern of CRH hnRNA and mRNA responses were similar, decreasing with increasing frequency of exposure to the stressor, while AVP mRNA responses increased in response to repeated stress. 5 The gradual emergence of increased AVP transcription at a time of diminishing CRH response suggests that repeated stress results in a specific facilitation of AVP gene expression, perhaps by impairment of corticosterone feedback.