Linked Life Data

11215156

Source:http://linkedlifedata.com/resource/pubmed/id/11215156

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2001-2-15
pubmed:abstractText
Chronic mild or moderate stress elicits an adaptive change in central nervous systems that function to maintain homeostasis. The principal components of stress response are the extrahypothalamic corticotropin-releasing hormone (CRH) and the locus coeruleus (LC)-norepinephrine (NE) systems. CRH is known to produce various stress-, anxiety- and arousal-associated behaviors in animals. Moreover, CRH causes an increase in the firing rate and activity of tyrosine hydroxylase in the LC, and NE release in LC projection areas. It is thought that chronic inescapable and unpredictable stress can result in a sustained dysregulation of both CRH neuronal activity and LC-NE systems. One may hypothesize that the NE-CRH interaction occurs in the terminal projection of forebrain NE systems, the hypothalamic paraventricular nucleus (PVN), the bed nucleus of the stria terminalis (BNST) and the central nucleus of the amygdala (CeA) where NE stimulates CRH release. Such CRH-NE-CRH feed-forward systems elicit progressive augmentation of stress responsivity with repeated exposure. The beta-adrenergic receptor down-regulation is induced by acute and chronic exposure to moderate and predictable stress, implying an adaptation to stress. However, chronic unpredictable (variable) stress (CVS), a model for depression, up-regulated the beta-AR. In our laboratory, we found that concurrent treatment with the selective serotonin reuptake inhibitor (SSRI) citalopram caused beta-R down-regulation in the frontal cortex of rats treated with CVS for 14 days. As previously reported by the authors, an increase in 5-HT availability plays a role in preserving beta-R down-regulation by NE potentiating agents. In depressed patients, hyperactivation of the CRH-NE systems caused by the CRH-NE feed-forward system is thought to be involved in generating anxiety, sympathetic activation and hyperarousal. Moreover, a decrease in the 5-HT turnover in depressed patients has been reported. Accordingly, it is proposed that an increase in 5-HT availability by SSRI might contribute to normalize beta-R down-regulation as an adaptive regulatory mechanism against excessive CRH-NE neurotransmission under a "stressful" situation.
pubmed:language
jpn
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
1340-2544
pubmed:author
pubmed:issnType
Print
pubmed:volume
20
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
97-105
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
2000
pubmed:articleTitle
[Influences of chronic stress on central nervous systems].
pubmed:affiliation
Department of Neuropsychiatry, St. Marianna University School of Medicine, 2-16-1, Sugao, Miyamae-ku, Kawasaki, 216-8511 Japan.
pubmed:publicationType
Journal Article, English Abstract, Review