Deletion of the Autism-Associated Protein SHANK3 Abolishes Structural Synaptic Plasticity after Brain Trauma.

ABSTRACT: Autism spectrum disorders (ASDs) are characterized by repetitive behaviors and impairments of sociability and communication. About 1% of ASD cases are caused by mutations of SHANK3, a major scaffolding protein of the postsynaptic density. We studied the role of SHANK3 in plastic changes of excitatory synapses within the central nervous system by employing mild traumatic brain injury (mTBI) in WT and Shank3 knockout mice. In WT mice, mTBI triggered ipsi- and contralateral loss of hippocampal dendritic spines and excitatory synapses with a partial recovery over time. In contrast, no significant synaptic alterations were detected in Shank3∆11-/- mice, which showed fewer dendritic spines and excitatory synapses at baseline. In line, mTBI induced the upregulation of

SUBMITTER: Urrutia-Ruiz C 

PROVIDER: S-EPMC9181590 | biostudies-literature | 2022 May

REPOSITORIES: biostudies-literature