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Reduced Prefrontal Synaptic Connectivity and Disturbed Oscillatory Population Dynamics in the CNTNAP2 Model of Autism
Maria T Lazaro1, Jiannis Taxidis2, Tristan Shuman3
1Interdepartmental Program for Neuroscience, UCLA, Los Angeles, CA, USA; Center for Neurobehavioral Genetics, Semel Institute, UCLA, Los Angeles, CA, USA; Department of Neurology, David Geffen School of Medicine, UCLA, Los Angeles, CA, USA.
Cell Reports
|May 30, 2019
Summary
Loss-of-function mutations in CNTNAP2 disrupt synaptic connections in the brain, leading to altered neuronal activity and communication. This impacts social behaviors and may explain autism spectrum disorder symptoms.
Area of Science:
- Neuroscience
- Genetics
- Developmental Biology
Background:
- Loss-of-function mutations in CNTNAP2 are linked to autism spectrum disorder (ASD) in humans, causing social deficits, repetitive behaviors, and seizures.
- The precise cellular and circuit-level mechanisms underlying these neurodevelopmental consequences remain poorly understood.
Purpose of the Study:
- To investigate the functional impact of Cntnap2 loss on neuronal connectivity and activity in the medial prefrontal cortex (mPFC).
- To elucidate how CNTNAP2 mutations affect synaptic function and neuronal network dynamics relevant to ASD.
Main Methods:
- Utilized laser-scanning photostimulation and whole-cell recordings in Cntnap2 knockout (KO) mice.
- Employed electron microscopy to analyze synaptic structures.
- Recorded medial prefrontal cortex (mPFC) local field potentials (LFPs) and unit spiking in vivo.
Main Results:
- Observed a significant reduction in both excitatory and inhibitory synaptic inputs onto L2/3 pyramidal neurons in Cntnap2 KO mice.
- Found decreased spine and synapse density, despite normal dendritic complexity and intrinsic neuronal excitability.
- Detected increased inhibitory neuron activity, altered phase-locking to brain oscillations (delta and theta), and increased pairwise correlations during immobility in KO mice.
Conclusions:
- Reduced synaptic inputs in Cntnap2 KO mice disrupt the temporal coordination of neuronal firing within cortical networks.
- These findings provide a cellular and circuit-level explanation for behavioral deficits associated with CNTNAP2 mutations and ASD.
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