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Nat Neurosci. 2018 Jun;21(6):803-807. doi: 10.1038/s41593-018-0151-z. Epub 2018 May 21.

Chronic CRH depletion from GABAergic, long-range projection neurons in the extended amygdala reduces dopamine release and increases anxiety.

Author information

1
Department of Stress Neurobiology and Neurogenetics, Max Planck Institute of Psychiatry, Munich, Germany.
2
Department of Psychiatry, Harvard Medical School and McLean Hospital, Belmont, MA, USA.
3
Laboratory of Neuropsychopharmacology, Paulista State University, Araraquara, Brazil.
4
Schaller Research Group on Neuropeptides, German Cancer Research Center, Central Institute of Mental Health, University of Heidelberg, Heidelberg, Germany.
5
Institute of Developmental Genetics, Helmholtz Zentrum München, Munich, Germany.
6
Technische Universität München, Chair of Developmental Genetics, Munich, Germany.
7
German Center for Neurodegenerative Diseases (DZNE), Site Munich, Munich, Germany.
8
Instituto de Investigacion en Biomedicina de Buenos Aires (IBioBA)-CONICET-Partner Institute of the Max Planck Society, Buenos Aires, Argentina.
9
Department of Stress Neurobiology and Neurogenetics, Max Planck Institute of Psychiatry, Munich, Germany. deussing@psych.mpg.de.

Abstract

The interplay between corticotropin-releasing hormone (CRH) and the dopaminergic system has predominantly been studied in addiction and reward, while CRH-dopamine interactions in anxiety are scarcely understood. We describe a new population of CRH-expressing, GABAergic, long-range-projecting neurons in the extended amygdala that innervate the ventral tegmental area and alter anxiety following chronic CRH depletion. These neurons are part of a distinct CRH circuit that acts anxiolytically by positively modulating dopamine release.

PMID:
29786085
DOI:
10.1038/s41593-018-0151-z
[Indexed for MEDLINE]

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