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Cntnap2 loss drives striatal neuron hyperexcitability and behavioral inflexibility
Katherine R Cording1,2, Emilie M Tu3, Hongli Wang2
1Helen Wills Neuroscience Institute, University of California, Berkeley, Berkeley, CA USA.
Biorxiv : the Preprint Server for Biology
|May 20, 2024
Summary
Loss of CNTNAP2 gene in mice leads to abnormal brain activity in striatal neurons, causing repetitive behaviors seen in autism spectrum disorder (ASD). This research sheds light on ASD
Area of Science:
- Neuroscience
- Genetics
- Developmental Biology
Background:
- Autism spectrum disorder (ASD) is characterized by social deficits and repetitive behaviors (RRBs).
- Striatal circuits are implicated in motor learning and habit formation, potentially contributing to RRBs in ASD.
- CNTNAP2 is a risk gene for syndromic ASD, and its loss in mice is linked to RRBs.
Purpose of the Study:
- To investigate how loss of CNTNAP2 impacts striatal neuron function.
- To determine if altered striatal neuron activity contributes to ASD-relevant motor behaviors in Cntnap2 knockout mice.
Main Methods:
- Utilized Cntnap2 knockout (Cntnap2-/-) mice models.
- Examined cortical drive of direct pathway striatal projection neurons (dSPNs).
- Assessed intrinsic excitability of dSPNs and observed behavioral phenotypes.
Main Results:
- Cntnap2-/- mice showed increased cortical drive of dSPNs.
- Enhanced intrinsic excitability of dSPNs was observed in Cntnap2-/- mice.
- These mice displayed spontaneous repetitive behaviors, enhanced motor routine learning, perseveration, and cognitive inflexibility.
Conclusions:
- Increased corticostriatal drive of the direct pathway may underlie repetitive and inflexible behaviors in Cntnap2-/- mice.
- Altered striatal neuron activity is a potential mechanism contributing to RRBs in ASD.
- This study provides insights into the neurobiological underpinnings of ASD-associated repetitive behaviors.
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