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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)
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Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
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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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter 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
ISSN (print) / ISBN 0306-4522
e-ISSN 1873-7544
Zeitschrift Neuroscience
Quellenangaben Band: 159, Heft: 2, Seiten: 610-617 Artikelnummer: , Supplement: ,
Verlag International Brain Research Organization, Elsevier
Begutachtungsstatus Peer reviewed