Linked Life Data

11337130

Source:http://linkedlifedata.com/resource/pubmed/id/11337130

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2001-5-4
pubmed:abstractText
Exposure to chronic stress is thought to play an important role in the etiology of depression. In this disorder, a disrupted negative feedback response to exogenous glucocorticoids on cortisol secretion has been indicated. However, the regulation of glucocorticoid negative feedback by chronic stress is not fully understood. In the present study, we investigated the effects of chronic stress administered by water immersion and restraint (2 h/day) for four weeks on the glucocorticoid feedback in rats. In the acutely (one-time) stressed rats, the basal plasma corticosterone (CORT) level was markedly elevated, remained at high levels for 5 h after the termination of stress, and then decreased. In the chronically stressed rats, the CORT level was initially elevated similarly, but rapidly decreased at 2 h. In the dexamethasone (DEX) suppression test, the peak CORT level in response to stress was not suppressed by DEX in the acutely stressed rats, but was significantly suppressed in the chronically stressed rats. In contrast, the suppressive effects of DEX on the basal CORT secretion in naive rats were attenuated in the chronically stressed rats. In the chronically stressed hippocampus, which plays an important role in the regulation of the glucocorticoid feedback response, the binding of [3H]DEX was decreased and the increased response of activator protein-1 induced by acute stress was abolished. These results suggest that chronic stress induces a hypersuppressive state for induced CORT secretion in response to acute stress, which is caused by partial habituation, coping, and adaptation to the stressor, whereas it induces a hyposuppressive state for the basal CORT secretion, which is caused by glucocorticoid receptor downregulation. These mechanisms may be involved in the stress-induced neural abnormalities observed in depression.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0306-4530
pubmed:author
pubmed:issnType
Print
pubmed:volume
26
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
443-59
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:11337130-Adrenal Glands, pubmed-meshheading:11337130-Animals, pubmed-meshheading:11337130-Body Weight, pubmed-meshheading:11337130-Chronic Disease, pubmed-meshheading:11337130-Corticosterone, pubmed-meshheading:11337130-Dexamethasone, pubmed-meshheading:11337130-Down-Regulation, pubmed-meshheading:11337130-Feedback, pubmed-meshheading:11337130-Glucocorticoids, pubmed-meshheading:11337130-Hippocampus, pubmed-meshheading:11337130-Immersion, pubmed-meshheading:11337130-Kinetics, pubmed-meshheading:11337130-Male, pubmed-meshheading:11337130-Organ Size, pubmed-meshheading:11337130-Rats, pubmed-meshheading:11337130-Rats, Wistar, pubmed-meshheading:11337130-Receptors, Glucocorticoid, pubmed-meshheading:11337130-Restraint, Physical, pubmed-meshheading:11337130-Stress, Physiological, pubmed-meshheading:11337130-Thymus Gland, pubmed-meshheading:11337130-Transcription Factor AP-1
pubmed:year
2001
pubmed:articleTitle
Chronic stress differentially regulates glucocorticoid negative feedback response in rats.
pubmed:affiliation
Pharmacology Department, Central Research Laboratories, Tsumura and Co., 3586 Yoshiwara, Ami-machi, Inashiki-gun, 300-1192, Ibaraki, Japan. mizoguchi_kazushige@mail.tsumura.co.jp
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't