50‐kHz ultrasonic vocalizations do not signal social anhedonia in transgenic DISC1 rats

Abstract

Abstract Patients diagnosed with neuropsychiatric disorders, such as autism and schizophrenia, suffer from disorganized speech. The disrupted‐in‐schizophrenia 1 (DISC1) protein pathway is considered a risk factor for the development of several psychiatric disorders and plays an important role in the dysregulation of dopamine (DA), which in turn plays an important role in the regulation of ultrasonic vocalizations (USVs) in rats. Moreover, the DISC1 protein pathway has been identified as a cause of social anhedonia, that is, a decrease in the drive for social interactions. USVs transmit specific affective information to other rats, with 50‐kHz calls indicating a positive affective state in rats. Dysregulation of the dopaminergic system impacts the qualitative and quantitative features of USVs, such as duration, peak frequency, and the call rate. In this study, we thus used a well‐established transgenic DISC1 (tgDISC1) rat line to investigate whether the neural (decreased DA levels in the dorsal striatum, amygdala, and hippocampus (HPC)) and behavioral (social anhedonia) features of tgDISC1 rats could be manifested through the modulation of their 50‐kHz USVs. Analyses of three features (call rate, duration, and peak frequency) of all 50‐kHz revealed no significant differences between groups, suggesting decreased DA levels in the dorsal striatum and amygdala, and HPC may affect social interaction but leave 50‐kHz USV production intact.

Keywords

• DISC1
• 50-kHz USVs
• social reward
• non‐social reward
• social anhedonia