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Abstract
The top-ranked cross-disorder risk gene CACNA1C is strongly associated with multiple neuropsychiatric dysfunctions. In a recent series of studies, we applied a genomically informed approach and contributed extensively to the behavioral characterization of a genetic rat model haploinsufficient for the cross-disorder risk gene Cacna1c. Because deficits in processing social signals are associated with reduced social functioning as commonly seen in neuropsychiatric disorders, we focused on socio-affective communication through 22-kHz and 50-kHz ultrasonic vocalizations (USV). Specifically, we applied a reciprocal approach for studying socio-affective communication in sender and receiver by including rough-and-tumble play and playback of 22-kHz and 50-kHz USV. Here, we review the findings obtained in this recent series of studies and link them to the key features of 50-kHz USV emission during rough-and-tumble play and social approach behavior evoked by playback of 22-kHz and 50-kHz USV. We conclude that Cacna1c haploinsufficiency in rats leads to robust deficits in socio-affective communication through 22-kHz and 50-kHz USV and associated alterations in social behavior, such as rough-and-tumble play behavior.
Highlights
The top-ranked cross-disorder risk gene CACNA1C is strongly associated with multiple neuropsychiatric dysfunctions
In a significant subset of our studies, we focused on social behavior and ultrasonic vocalizations because reduced social functioning was associated with CACNA1C Single-nucleotide polymorphisms (SNPs) and is commonly seen in neuropsychiatric disorders in humans [15,16,17,18,19]
We further demonstrated for the first time that 50-kHz ultrasonic vocalizations (USV) typically emitted by juvenile and adult rats in appetitive social interactions, such as rough-and-tumble play, evoke social approach behavior, indicating that 50-kHz USV serve as social contact calls [88]
Summary
The top-ranked cross-disorder risk gene CACNA1C is strongly associated with multiple neuropsychiatric dysfunctions. In a recent series of studies, we applied a genomically informed approach and contributed extensively to the behavioral characterization of a genetic rat model haploinsufficient for the cross-disorder risk gene Cacna1c [13,14,15,16,17,18,19], flanked by neurobiological analyses [20,21,22,23] In this rat model, Cav1.2 expression in the brain is reduced to about 50% of wildtype littermate controls, both in males [15] and females [16]. Verbal fluency was reported to be reduced in CACNA1C SNP risk carriers [27]
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