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Refojo, D.* ; Schweizer, M.* ; Kuehne, C.* ; Ehrenberg, S.* ; Thoeringer, C.* ; Vogl, A.M.* ; Dedic, N.* ; Schumacher, M.* ; von Wolff, G.* ; Avrabos, C.* ; Touma, C.* ; Engblom, D.* ; Schütz, G.* ; Nave, K.A.* ; Eder, M.* ; Wotjak, C.T.* ; Sillaber, I.* ; Holsboer, F.* ; Wurst, W. ; Deussing, J.M.*

Glutamatergic and dopaminergic neurons mediate anxiogenic and anxiolytic effects of CRHR1.

Science 333, 1903-1907 (2011)
Verlagsversion Verlagsversion DOI
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
The corticotropin-releasing hormone receptor 1 (CRHR1) critically controls behavioral adaptation to stress and is causally linked to emotional disorders. Using neurochemical and genetic tools, we determined that CRHR1 is expressed in forebrain glutamatergic and γ-aminobutyric acid-containing (GABAergic) neurons as well as in midbrain dopaminergic neurons. Via specific CRHR1 deletions in glutamatergic, GABAergic, dopaminergic, and serotonergic cells, we found that the lack of CRHR1 in forebrain glutamatergic circuits reduces anxiety and impairs neurotransmission in the amygdala and hippocampus. Selective deletion of CRHR1 in midbrain dopaminergic neurons increases anxiety-like behavior and reduces dopamine release in the prefrontal cortex. These results define a bidirectional model for the role of CRHR1 in anxiety and suggest that an imbalance between CRHR1-controlled anxiogenic glutamatergic and anxiolytic dopaminergic systems might lead to emotional disorders.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter no keywords
ISSN (print) / ISBN 0036-8075
e-ISSN 1095-9203
Zeitschrift Science
Quellenangaben Band: 333, Heft: 6051, Seiten: 1903-1907 Artikelnummer: , Supplement: ,
Verlag American Association for the Advancement of Science (AAAS)
Begutachtungsstatus Peer reviewed