Abstract
Social deficit is a major feature of neuropsychiatric disorders, including autism spectrum disorders, schizophrenia, and attention-deficit/hyperactivity disorder, but its neural mechanisms remain unclear. Here, we examined neuronal discharge characteristics in the medial prefrontal cortex (mPFC) of IRSp53-mutant mice, which show social deficits, during social approach. IRSp53-mutant excitatory mPFC neurons displayed an increase in baseline neuronal firing and decreases in variability and dynamic range of firing rates and burst firing during social and non-social target approaches compared to wild-type controls. As a consequence, their firing activity was less differential between social and non-social targets. In addition, there was a decrease in the proportion of excitatory mPFC neurons encoding social information but not that of those encoding non-social information. These results suggest that insufficient neuronal activity dynamics may underlie impaired cortical encoding of social information and social behaviors in IRSp53-mutant mice.
Competing Interest Statement
The authors have declared no competing interest.
Footnotes
Competing interests: Eunjoon Kim: Reviewing editor, eLife
Data Availability: Source Data files have been provided for all figures (except for Figure 1 - figure supplement 1). N/A
Ethics: Human Subjects: No Animal Subjects: Yes Ethics Statement: Mice were maintained according to the Animal Research Requirements of Korea Advanced Institute of Science and Technology (KAIST). All experiments were conducted with approval from the Committee on Animal Research at KAIST (approval number KA2020-94).
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