期刊
CEREBRAL CORTEX
卷 32, 期 21, 页码 4797-4817出版社
OXFORD UNIV PRESS INC
DOI: 10.1093/cercor/bhab517
关键词
auditory cortex; auditory processing; autism spectrum disorder; CASPR2; Cntnap2; evoked potentials; neurodevelopmental disorder; rat
资金
- Natural Sciences and Engineering Research Council Canada (NSERC) [RGPIN-2018-04472]
- Canadian Institute for Health Research (CIHR) [425659]
- Canadian First Research Excellence Funds (CFREF) (Brains CAN accelerator grant)
- Simons Foundation Autism Research Initiative (SFARI)
Loss of CNTNAP2 gene function in rats can cause auditory processing impairments similar to those seen in language-related human disorders, indicating its importance in maintaining cortical neuron excitability.
The contactin-associated protein-like 2 gene, CNTNAP2, is a highly penetrant risk gene thought to play a role in the genetic etiology of language-related disorders, such as autism spectrum disorder and developmental language disorder. Despite its candidacy for influencing language development, few preclinical studies have examined the role of CNTNAP2 in auditory processing. Using in vivo and in vitro electrophysiological recordings in a rat model with translational validity, we report that a loss of the Cntnap2 gene function caused immature-like cortical evoked potentials, delayed multiunit response latencies to acoustic stimuli, impaired temporal processing, and led to a pattern of hyperexcitability in both multiunit and single cell recordings in adulthood. These collective results provide direct evidence that a constitutive loss of Cntnap2 gene function in rats can cause auditory processing impairments similar to those seen in language-related human disorders, indicating that its contribution in maintaining cortical neuron excitability may underlie the cortical activity alterations observed in Cntnap2(-/-) rats.
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