Journal
PROGRESS IN NEUROBIOLOGY
Volume 91, Issue 1, Pages 23-37Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.pneurobio.2010.01.004
Keywords
NR3A; NMDA receptor; Synaptic plasticity; Neurodevelopmental disorders; Dendritic spine; NMDA subunit; LTP; Synapse elimination; Synapse maturation
Categories
Funding
- NARSAD
- NICHD [T32-HD40127]
- UTE
- Gobierno de Navarra, Spanish Ministry of Science [SAF2006-10025, CSI2008-00005]
- National Science Foundation [0822969]
- National Eye Institute [R01EY018323]
- UNC Charles Lee Raper Dissertation Fellowship
- Society for Neuroscience/NINDS
- EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT [T32HD040127] Funding Source: NIH RePORTER
- NATIONAL EYE INSTITUTE [R01EY018323] Funding Source: NIH RePORTER
- Medical Research Council [G0001354B, G0001354] Funding Source: researchfish
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Various combinations of subunits assemble to form the NMDA-type glutamate receptor (NMDAR), generating diversity in its functions. Here we review roles of the unique NMDAR subunit, NR3A, which acts in a dominant-negative manner to suppress receptor activity. NR3A-containing NMDARs display striking regional and temporal expression specificity, and, unlike most other NMDAR subtypes, they have a low conductance, are only modestly permeable to Ca2+, and pass current at hyperpolarized potentials in the presence of magnesium. While glutamate activates triheteromeric NMDARs composed of NR1/NR2/NR3A subunits, glycine is sufficient to activate diheteromeric NR1/NR3A-containing receptors. NR3A dysfunction may contribute to neurological disorders involving NMDARs, and the subunit offers an attractive therapeutic target given its distinct pharmacological and structural properties. (C) 2010 Elsevier Ltd. All rights reserved.
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