Cacna1c haploinsufficiency leads to pro-social 50-kHz ultrasonic communication deficits in rats

• Verfasst von: Kisko, Theresa Marie [VerfasserIn]
• Verfasst von: Witt, Stephanie [VerfasserIn]
• Verfasst von: Rietschel, Marcella [VerfasserIn]
• Titel: Cacna1c haploinsufficiency leads to pro-social 50-kHz ultrasonic communication deficits in rats
• Verf.angabe: Theresa M. Kisko, Moria D. Braun, Susanne Michels, Stephanie H. Witt, Marcella Rietschel, Carsten Culmsee, Rainer K.W. Schwarting and Markus Wöhr
• E-Jahr: 2018
• Jahr: June 20, 2018
• Umfang: 11 S.
• Fussnoten: Gesehen am 23.10.2019
• Titel Quelle: Enthalten in: Disease models & mechanisms
• Ort Quelle: Cambridge : Company of Biologists Limited, 2008
• Jahr Quelle: 2018
• Band/Heft Quelle: 11(2018), 6, Artikel-ID dmm034116, Seite 1-11
• ISSN Quelle: 1754-8411
• DOI: doi:10.1242/dmm.034116
• Datenträger: Online-Ressource
• Sprache: eng
• K10plus-PPN: 1679482041

Abstract

The cross-disorder risk gene CACNA1C is strongly implicated in multiple neuropsychiatric disorders, including autism spectrum disorder (ASD), bipolar disorder (BPD) and schizophrenia (SCZ), with deficits in social functioning being common for all major neuropsychiatric disorders. In the present study, we explored the role of Cacna1c in regulating disorder-relevant behavioral phenotypes, focusing on socio-affective communication after weaning during the critical developmental period of adolescence in rats.