
Cntnap2 유전자 결실은 선조체 투사 신경세포의 과도한 피질 입력 유발과 내재적 흥분성 증가를 통해 반복적이고 경직된 행동 양상을 초래한다.


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Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by two major diagnostic criteria - persistent deficits in social communication and interaction, and the presence of restricted, repetitive patterns of behavior (RRBs). Evidence from both human and animal model studies of ASD suggest that alteration of striatal circuits, which mediate motor learning, action selection, and habit formation, may contribute to the manifestation of RRBs. CNTNAP2 is a syndromic ASD risk gene, and loss of function of Cntnap2 in mice is associated with RRBs. How loss of Cntnap2 impacts striatal neuron function is largely unknown. In this study, we utilized Cntnap2-/- mice to test whether altered striatal neuron activity contributes to aberrant motor behaviors relevant to ASD. We find that Cntnap2-/- mice exhibit increased cortical drive of striatal projection neurons (SPNs), with the most pronounced effects in direct pathway SPNs. This enhanced drive is likely due to increased intrinsic excitability of SPNs, which make them more responsive to cortical inputs. We also find that Cntnap2-/- mice exhibit spontaneous repetitive behaviors, increased motor routine learning, and cognitive inflexibility. Increased corticostriatal drive, in particular of the direct pathway, may contribute to the acquisition of repetitive, inflexible behaviors in Cntnap2 mice.

### Competing Interest Statement

The authors have declared no competing interest.

Cntnap2 loss drives striatal neuron hyperexcitability and behavioral inflexibility

자폐-스펙트럼-장애-유발-유전자-cntnap2-결실이-선조체-신경세포의-과흥분성과-행동-경직성을-유발한다


자폐 스펙트럼 장애 유발 유전자 Cntnap2 결실이 선조체 신경세포의 과흥분성과 행동 경직성을 유발한다
