Microglial activation and increased microglial density observed in the dorsolateral prefrontal cortex in autism.
Molecular Mechanisms
Hypersensitivity to mGluR5 and ERK1/2 leads to excessive protein synthesis in the hippocampus of a mouse model of fragile X syndrome.
Fragile X mental retardation protein is required for synapse elimination by the activity-dependent transcription factor MEF2.
Mutations in PNKP cause microcephaly, seizures and defects in DNA repair.
Prenatal polycyclic aromatic hydrocarbon exposure leads to behavioral deficits and downregulation of receptor tyrosine kinase, MET.
Haploinsufficiency of the autism-associated SHANK3 gene leads to deficits in synaptic function, social interaction, and social communication.
Activation of mGluR5 induces rapid and long-lasting protein kinase D phosphorylation in hippocampal neurons.
A resource of Cre driver lines for genetic targeting of GABAergic neurons in cerebral cortex.
A presynaptic role for FMRP during protein synthesis-dependent long-term plasticity in Aplysia.
Foxp2 regulates gene networks implicated in neurite outgrowth in the developing brain.
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