CURRENT OPINION IN PHARMACOLOGY, v.20, no., pp.8 - 13
ELSEVIER SCI LTD
Abnormalities and imbalances in neuronal excitatory and
inhibitory synapses have been implicated in diverse
neuropsychiatric disorders including autism spectrum disorders
(ASDs). Increasing evidence indicates that dysfunction of NMDA
receptors (NMDARs) at excitatory synapses is associated with
ASDs. In support of this, human ASD-associated genetic
variations are found in genes encoding NMDAR subunits.
Pharmacological enhancement or suppression of NMDAR
function ameliorates ASD symptoms in humans. Animal models
of ASD display bidirectional NMDAR dysfunction, and correcting
this deficit rescues ASD-like behaviors. These findings suggest
that deviation of NMDAR function in either direction contributes
to the development of ASDs, and that correcting NMDAR
dysfunction has therapeutic potential for ASDs.