Linked Life Data

19361479

Source:http://linkedlifedata.com/resource/pubmed/id/19361479

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2009-4-16
pubmed:abstractText
Corticotropin-releasing hormone (CRH) coordinates neuroendocrine and behavioral adaptations to stress. Acute CRH administration in vivo activates extracellular signal-regulated kinase 1/2 (ERK1/2) in limbic brain areas, acting through the CRH receptor type 1 (CRH-R1). In the present study, we used CRH-COE-Cam mice that overexpress CRH in limbic-restricted areas, to analyze the effect of chronic CRH overexpression on ERK1/2 activation. By immunohistochemistry and confocal microscopy analysis we found that pERK1/2 levels in the basolateral amygdala (BLA) were similar in control and CRH overexpressing mice under basal conditions. Acute stress caused comparably increased levels of corticosterone in both control (CRH-COEcon-Cam) and CRH overexpressing (CRH-COEhom-Cam) animals. CRH-COEhom-Cam mice after stress showed reduced pERK1/2 immunoreactivity in the BLA compared to CRH-COEhom-Cam animals under basal conditions. Radioligand binding and in situ hybridization revealed higher density of CRH-R1 in the amygdala of CRH-COEhom mice under basal conditions compared to control littermates. A significant reduction of the receptor levels was observed in this area after acute stress, suggesting that stress may trigger CRH-R1 internalization/downregulation in these CRH overexpressing mice. Chronic CRH overexpression leads to reduced ERK1/2 activation in response to acute stress in the BLA.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0306-4522
pubmed:author
pubmed:issnType
Print
pubmed:day
17
pubmed:volume
159
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
610-7
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:19361479-Amphibian Proteins, pubmed-meshheading:19361479-Amygdala, pubmed-meshheading:19361479-Animals, pubmed-meshheading:19361479-Autoradiography, pubmed-meshheading:19361479-Corticosterone, pubmed-meshheading:19361479-Corticotropin-Releasing Hormone, pubmed-meshheading:19361479-Disease Models, Animal, pubmed-meshheading:19361479-Gene Expression Regulation, Enzymologic, pubmed-meshheading:19361479-Iodine Isotopes, pubmed-meshheading:19361479-Male, pubmed-meshheading:19361479-Mice, pubmed-meshheading:19361479-Mice, Transgenic, pubmed-meshheading:19361479-Mitogen-Activated Protein Kinase 3, pubmed-meshheading:19361479-Peptide Hormones, pubmed-meshheading:19361479-Protein Binding, pubmed-meshheading:19361479-Radioimmunoassay, pubmed-meshheading:19361479-Receptors, Corticotropin-Releasing Hormone, pubmed-meshheading:19361479-Restraint, Physical, pubmed-meshheading:19361479-Stress, Psychological, pubmed-meshheading:19361479-Time Factors
pubmed:year
2009
pubmed:articleTitle
Amygdaloid pERK1/2 in corticotropin-releasing hormone overexpressing mice under basal and acute stress conditions.
pubmed:affiliation
Laboratorio de Fisiología y Biología Molecular, Departamento de Fisiología y Biología y Celular, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires and IFIBYNE-CONICET, Ciudad Universitaria, Buenos Aires, Argenita.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't