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Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
Amygdaloid pERK1/2 in corticotropin-releasing hormone overexpressing mice under basal and acute stress conditions.
Neuroscience 159, 610-617 (2009)
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
Verlag
International Brain Research Organization, Elsevier
Nichtpatentliteratur
Publikationen
Begutachtungsstatus
Peer reviewed