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Silberstein, S.* ; Vogl, A.M.* ; Refojo, D.* ; Senin, S.A.* ; Wurst, W. ; Holsboer, F.* ; Deussing, J.M.* ; Arzt, E.*

Amygdaloid pERK1/2 in corticotropin-releasing hormone overexpressing mice under basal and acute stress conditions.

Neuroscience 159, 610-617 (2009)
DOI PMC
Open Access Green as soon as Postprint is submitted to ZB.
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.
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Publication type Article: Journal article
Document type Scientific Article
Keywords HPA axis; CRH; CRF; CRH receptor; ERK; activated protein-kinases; central-nervous-system; rat-brain; factor-receptor; map kinase; synaptic plasticity; transgenic mice; messenger-rnas; crf receptors; swim stress
Language english
Publication Year 2009
HGF-reported in Year 2009
ISSN (print) / ISBN 0306-4522
e-ISSN 1873-7544
Journal Neuroscience
Quellenangaben Volume: 159, Issue: 2, Pages: 610-617 Article Number: , Supplement: ,
Publisher International Brain Research Organization, Elsevier
Reviewing status Peer reviewed
POF-Topic(s) 30204 - Cell Programming and Repair
30504 - Mechanisms of Genetic and Environmental Influences on Health and Disease
Research field(s) Genetics and Epidemiology
PSP Element(s) G-500500-001
G-520600-001
Scopus ID 61349189527
PubMed ID 19361479
Erfassungsdatum 2009-07-09