The N-Methyl-D-Aspartate (NMDA) receptor complex is comprised of 2 types of subunits, NR1 and NR2. Only one type of NR1 subunits has yet been identified while four distinct subunits have been identified for the NR2 receptor, NR2A, NR2B, NR2C, and NR2D. While the NR2 subunits are not functional alone, they combine with the NR1 subunit to produce a variety of different receptor types. A number have studies have also shown that the functional properties of the receptors complexes formed by the NR1 and NR2 subunits are largely determined by the NR2 components of the complex. NMDA receptors are post-synaptic and play important roles in plasticity in the developing and mature central nervous system (CNS). Agonists and antagonists of NMDA receptors have been proposed to be of therapeutic benefit in a number of CNS disorders, including stroke, head injury, epilepsy, pain, and Alzheimer′s disease.
N-methyl-D-aspartate (NMDA) receptors are a class of ionotropic glutamate-gated ion channels. These receptors have been shown to be involved in long-term potentiation, an activity-dependent increase in the efficiency of synaptic transmission thought to underlie certain kinds of memory and learning. NMDA receptor channels are heteromers composed of the key receptor subunit NMDAR1 (GRIN1) and 1 or more of the 4 NMDAR2 subunits: NMDAR2A (GRIN2A), NMDAR2B (GRIN2B), NMDAR2C (GRIN2C) and NMDAR2D (GRIN2D).N-methyl-D-aspartate (NMDA) receptors are a class of ionotropic glutamate receptors. NMDA channel has been shown to be involved in long-term potentiation, an activity-dependent increase in the efficiency of synaptic transmission thought to underlie certain kinds of memory and learning. NMDA receptor channels are heteromers composed of the key receptor subunit NMDAR1 (GRIN1) and 1 or more of the 4 NMDAR2 subunits: NMDAR2A (GRIN2A), NMDAR2B (GRIN2B), NMDAR2C (GRIN2C), and NMDAR2D (GRIN2D). Publication Note: This RefSeq record includes a subset of the publications th at are available for this gene. Please see the Entrez Gene record to access additional publications.