Excessive Formation and Stabilization of Dendritic Spine Clusters in the <i>MECP2</i>-Duplication Syndrome Mouse Model of Autism
Ryan T. Ash, Jiyoung Park, Bernhard Suter, Huda Y. Zoghbi, Stelios M. Smirnakis
Abstract
Autism-associated genetic mutations may perturb the balance between stability and plasticity of synaptic connections in the brain. Here, we report an increase in the formation and stabilization of dendritic spines in the cerebral cortex of the mouse model of MECP2-duplication syndrome, a high-penetrance form of syndromic autism. Increased stabilization is mediated entirely by spines that form cooperatively in 10-mm clusters and is observable across multiple cortical areas both spontaneously and following motor training. Excessive stability of dendritic spine clusters could contribute to behavioral rigidity and other phenotypes in syndromic autism.
Topics & Concepts
Dendritic spineAutismMECP2NeuroscienceGene duplicationSPINE (molecular biology)NeuroliginPhenotypeBiologyPsychologyGeneticsExcitatory postsynaptic potentialInhibitory postsynaptic potentialGeneCell biologyPsychiatryHippocampal formationGenetics and Neurodevelopmental DisordersAutism Spectrum Disorder ResearchNeurogenesis and neuroplasticity mechanisms