Autism-Associated Shank3 Is Essential for Homeostatic Compensation in Rodent V1.
Ontology highlight
ABSTRACT: Mutations in Shank3 are strongly associated with autism spectrum disorders and neural circuit changes in several brain areas, but the cellular mechanisms that underlie these defects are not understood. Homeostatic forms of plasticity allow central circuits to maintain stable function during experience-dependent development, leading us to ask whether loss of Shank3 might impair homeostatic plasticity and circuit-level compensation to perturbations. We found that Shank3 loss in vitro abolished synaptic scaling and intrinsic homeostatic plasticity, deficits that could be rescued by treatment with lithium. Further, Shank3 knockout severely compromised the in vivo ability of visual cortical circuits to recover from perturbations to sensory drive. Finally, lithium treatment ameliorated a repetit
SUBMITTER: Tatavarty V
PROVIDER: S-EPMC7331792 | biostudies-literature | 2020 Jun
REPOSITORIES: biostudies-literature
ACCESS DATA