Molecular Mechanisms

Neuroligin-1 performs neurexin-dependent and neurexin-independent functions in synapse validation.

Intrinsic patterning and experience-dependent mechanisms that generate eye-specific projections and binocular circuits in the visual pathway.

Genetic fate mapping reveals that the caudal ganglionic eminence produces a large and diverse population of superficial cortical interneurons.

Microglial activation and increased microglial density observed in the dorsolateral prefrontal cortex in autism.

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.

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