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Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
Conditional mouse mutants highlight mechanisms of corticotropin-releasing hormone effects on stress-coping behavior.
Mol. Psychiatry 13, 1028-1042 (2008)
Hypersecretion of central corticotropin-releasing hormone (CRH) has been implicated in the pathophysiology of affective disorders. Both, basic and clinical studies suggested that disrupting CRH signaling through CRH type 1 receptors (CRH-R1) can ameliorate stress-related clinical conditions. To study the effects of CRH-R1 blockade upon CRH-elicited behavioral and neurochemical changes we created different mouse lines overexpressing CRH in distinct spatially restricted patterns. CRH overexpression in the entire central nervous system, but not when overexpressed in specific forebrain regions, resulted in stress-induced hypersecretion of stress hormones and increased active stress-coping behavior reflected by reduced immobility in the forced swim test and tail suspension test. These changes were related to acute effects of overexpressed CRH as they were normalized by CRH-R1 antagonist treatment and recapitulated the effect of stress-induced activation of the endogenous CRH system. Moreover, we identified enhanced noradrenergic activity as potential molecular mechanism underlying increased active stress-coping behavior observed in these animals. Thus, these transgenic mouse lines may serve as animal models for stress-elicited pathologies and treatments that target the central CRH system.
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Publikationstyp
Artikel: Journalartikel
Dokumenttyp
Wissenschaftlicher Artikel
Schlagwörter
corticotropin-releasing hormone; depression; forced swim test; HPA axis; ROSA26; DMP696
ISSN (print) / ISBN
1359-4184
e-ISSN
1476-5578
Zeitschrift
Molecular Psychiatry
Quellenangaben
Band: 13,
Heft: 11,
Seiten: 1028-1042
Verlag
Springer
Begutachtungsstatus
Peer reviewed
Institut(e)
Institute of Developmental Genetics (IDG)