Cell
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Somatosensory over-reactivity is common among patients with autism spectrum disorders (ASDs) and is hypothesized to contribute to core ASD behaviors. However, effective treatments for sensory over-reactivity and ASDs are lacking. We found distinct somatosensory neuron pathophysiological mechanisms underlie tactile abnormalities in different ASD mouse models and contribute to some ASD-related behaviors. ⋯ Moreover, acute treatment with a peripherally restricted GABAA receptor agonist that acts directly on mechanosensory neurons reduced tactile over-reactivity in six distinct ASD models. Chronic treatment of Mecp2 and Shank3 mutant mice improved body condition, some brain abnormalities, anxiety-like behaviors, and some social impairments but not memory impairments, motor deficits, or overgrooming. Our findings reveal a potential therapeutic strategy targeting peripheral mechanosensory neurons to treat tactile over-reactivity and select ASD-related behaviors.
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Autism spectrum disorder (ASD) is prevalent, complex, and heterogeneous, and currently there is no cure. Identifying shared mechanisms across the ASD spectrum is of utmost importance for therapeutic intervention. Orefice et al. show that tackling the GABAA receptor pathway in the peripheral somatosensory system in various ASD mouse models rescues core ASD-like phenotypes.