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Disruption of the human  SHANK3  gene can cause several neuropsychiatric disease entities including Phelan-McDermid syndrome, autism spectrum disorder (ASD), and intellectual disability. Although, a wide array of neurobiological studies strongly supports a major role for SHANK3 in organizing the post-synaptic protein scaffold, the molecular processes at synapses of individuals harboring  SHANK3  mutations are still far from being understood. In this study, we biochemically isolated the post-synaptic density (PSD) fraction from striatum and hippocampus of adult  Shank3Δ11 -/-   mutant mice and performed ion-mobility enhanced data-independent label-free LC–MS/MS to obtain the corresponding PSD proteomes (Data are available via ProteomeXchange with identifier PXD005192). This unbiased approach to identify molecular disturbances at  Shank3  mutant PSDs revealed hitherto unknown brain region specific alterations including a striatal decrease of several molecules encoded by ASD susceptibility genes such as the serine/threonine kinase Cdkl5 and the potassium channel K Ca 1.1. Being the first comprehensive analysis of brain region specific PSD proteomes from a  Shank3  mutant line, our study provides crucial information on molecular alterations that could foster translational treatment studies for  SHANK3  mutation-associated synaptopathies and possibly also ASD in general.

frontiers in molecular neuroscience

Proteomic Analysis of Post-synaptic Density Fractions from Shank3 Mutant Mice Reveals Brain Region Specific Changes Relevant to Autism Spectrum Disorder