Sex-dependent effects of Cacna1c haploinsufficiency on behavioral inhibition evoked by conspecific alarm signals in rats.


Journal

Progress in neuro-psychopharmacology & biological psychiatry
ISSN: 1878-4216
Titre abrégé: Prog Neuropsychopharmacol Biol Psychiatry
Pays: England
ID NLM: 8211617

Informations de publication

Date de publication:
20 04 2020
Historique:
received: 16 09 2019
revised: 13 12 2019
accepted: 16 12 2019
pubmed: 22 12 2019
medline: 1 4 2021
entrez: 22 12 2019
Statut: ppublish

Résumé

Deficits in processing social signals leads to reduced social functioning and is typically associated with neuropsychiatric disorders, including autism spectrum disorder, schizophrenia, and major depressive disorder. The cross-disorder risk gene CACNA1C is implicated in the etiology of all of these disorders and single-nucleotide polymorphisms within CACNA1C are ranked among the best replicated and most robust genetic findings from genome-wide association studies in psychiatry. Rats are highly social, live in large social groups, and communicate through ultrasonic vocalizations (USV), with low-frequency 22-kHz USV emitted in dangerous and often life-threating situations, such as predator exposure, serving an alarming function. In the present study, we applied an alarm 22-kHz USV playback paradigm to investigate the role of Cacna1c in socio-affective information processing in rats. Specifically, we assessed behavioral inhibition evoked by 22-kHz USV in constitutive heterozygous Cacna1c

Identifiants

pubmed: 31862418
pii: S0278-5846(19)30778-X
doi: 10.1016/j.pnpbp.2019.109849
pii:
doi:

Substances chimiques

Cacna1c protein, rat 0
Calcium Channels, L-Type 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

109849

Informations de copyright

Copyright © 2019 Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of Competing Interest M.W. is scientific advisor of Avisoft Bioacoustics. The other authors declare no competing interests.

Auteurs

Markus Wöhr (M)

Behavioral Neuroscience, Experimental and Biological Psychology, Department of Psychology, Philipps-Universität Marburg, Gutenbergstr. 18, D-35032 Marburg, Germany; Center for Mind, Brain, and Behavior (CMBB), Philipps-Universität Marburg, Hans-Meerwein-Str. 6, D-35032 Marburg, Germany. Electronic address: markus.woehr@staff.uni-marburg.de.

Maria Willadsen (M)

Behavioral Neuroscience, Experimental and Biological Psychology, Department of Psychology, Philipps-Universität Marburg, Gutenbergstr. 18, D-35032 Marburg, Germany.

Theresa M Kisko (TM)

Behavioral Neuroscience, Experimental and Biological Psychology, Department of Psychology, Philipps-Universität Marburg, Gutenbergstr. 18, D-35032 Marburg, Germany.

Rainer K W Schwarting (RKW)

Behavioral Neuroscience, Experimental and Biological Psychology, Department of Psychology, Philipps-Universität Marburg, Gutenbergstr. 18, D-35032 Marburg, Germany; Center for Mind, Brain, and Behavior (CMBB), Philipps-Universität Marburg, Hans-Meerwein-Str. 6, D-35032 Marburg, Germany.

Markus Fendt (M)

Institute for Pharmacology and Toxicology, Otto-von-Guericke University Magdeburg, Leipziger Str. 44, D-39120 Magdeburg, Germany; Center for Behavioral Brain Sciences, Otto-von-Guericke University Magdeburg, Leipziger Str. 44, D-39120 Magdeburg, Germany.

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Classifications MeSH