Fig. 3. The striatal dysfunction hypothesis of autistic-like behaviors. (A) Optogenetic stimulation of the glutamatergic inputs from the prefrontal cortex (PL) to the dorsal striatum (dST) suppressed social interaction with a social novelty and novel object preference [5]. Similarly, optogenetic stimulation of the dopaminergic inputs from the substantia nigra (SN) to the dorsal striatum reduced social interaction [6]. (B) A list of the genes whose dysfunction in the dorsal striatum produced autistic-like behaviors. Molecular, genetic, and pharmacological data suggest that increased activity of mGluR5, D1, ERK1/2, CaMKIIα, or mTOR or decreased activity of mGluR3, GluN2B, GluA1, SHANK3, NLGN3, D2, DAT, TSC1/2, MeCP2, or FMR1 promoted pro-autistic behaviors. References are indicated.
