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Curr Opin Pharmacol. 2015 Feb;20:8-13. doi: 10.1016/j.coph.2014.10.007. Epub 2015 Jan 28.

NMDA receptor dysfunction in autism spectrum disorders.

Author information

1
Graduate School of Medical Science and Engineering, Korea Advanced Institute of Science and Technology (KAIST), Daejeon 305-701, Republic of Korea.
2
Department of Biological Sciences, KAIST, Daejeon 305-701, Republic of Korea.
3
Department of Biological Sciences, KAIST, Daejeon 305-701, Republic of Korea; Center for Synaptic Brain Dysfunctions, Institute for Basic Science (IBS), Daejeon 305-701, Republic of Korea. Electronic address: kime@kaist.ac.kr.

Abstract

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.

PMID:
25636159
DOI:
10.1016/j.coph.2014.10.007
[Indexed for MEDLINE]

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