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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2002-2-25
pubmed:abstractText
In a series of experiments, we tested the hypothesis that chronic antidepressant drug administration reduces the synaptic availability of corticotropin-releasing factor (CRF) through one or more effects on CRF gene expression or peptide synthesis. We also determined whether effects of acute or chronic stress on CRF gene expression or peptide concentration are influenced by antidepressant drug treatment. Four-week treatment with venlafaxine, a dual serotonin (5-HT)/norepinephrine (NE) reuptake inhibitor, and tranylcypromine, a monoamine oxidase inhibitor, resulted in an attenuation of acute stress-induced increases in CRF heteronuclear RNA (hnRNA) synthesis in the paraventricular nucleus (PVN). Trends toward the same effect were observed after treatment with the 5-HT reuptake inhibitor fluoxetine, or the NE reuptake inhibitor reboxetine. CRF mRNA accumulation in the PVN during exposure to chronic variable stress was attenuated by concurrent antidepressant administration. Basal CRF hnRNA and mRNA expression were not affected by antidepressant treatment in the PVN or in other brain regions examined. Chronic stress reduced CRF concentrations in the median eminence, but there were no consistent effects of antidepressant drug treatment on CRF, serum corticotropin, or corticosterone concentrations. CRF receptor expression and basal and stress-stimulated HPA axis activity were unchanged after antidepressant administration. These results suggest that chronic antidepressant administration diminishes the sensitivity of CRF neurons to stress rather than alters their basal activity. Additional studies are required to elucidate the functional consequences and mechanisms of this interaction.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0022-3565
pubmed:author
pubmed:issnType
Print
pubmed:volume
300
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1085-92
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:11861819-Adrenocorticotropic Hormone, pubmed-meshheading:11861819-Animals, pubmed-meshheading:11861819-Antidepressive Agents, pubmed-meshheading:11861819-Autoradiography, pubmed-meshheading:11861819-Corticotropin-Releasing Hormone, pubmed-meshheading:11861819-Hypothalamo-Hypophyseal System, pubmed-meshheading:11861819-Immobilization, pubmed-meshheading:11861819-In Situ Hybridization, pubmed-meshheading:11861819-Male, pubmed-meshheading:11861819-Neurons, pubmed-meshheading:11861819-Pituitary-Adrenal System, pubmed-meshheading:11861819-RNA, Antisense, pubmed-meshheading:11861819-RNA, Messenger, pubmed-meshheading:11861819-RNA Processing, Post-Transcriptional, pubmed-meshheading:11861819-Radioimmunoassay, pubmed-meshheading:11861819-Rats, pubmed-meshheading:11861819-Rats, Sprague-Dawley, pubmed-meshheading:11861819-Receptors, Corticotropin-Releasing Hormone, pubmed-meshheading:11861819-Stress, Psychological, pubmed-meshheading:11861819-Swimming
pubmed:year
2002
pubmed:articleTitle
Regulation of corticotropin-releasing factor neuronal systems and hypothalamic-pituitary-adrenal axis activity by stress and chronic antidepressant treatment.
pubmed:affiliation
Laboratory of Neuropsychopharmacology, Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, Georgia 30322, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't