Glutamate [N-methyl-D-aspartate] receptor subunit 2B (GluN2B)

The **GluN2B NMDA receptor** (Glutamate [N-methyl-D-aspartate] receptor subunit 2B) is a subunit of the NMDA-type glutamate receptors, which are ligand-gated ion channels mediating calcium-permeable excitatory neurotransmission in the central nervous system[1][3][7]. NMDA receptors are typically heterotetramers composed of two GluN1 and two GluN2 subunits, with GluN2B conferring specific biophysical properties such as higher calcium permeability and sensitivity to voltage-dependent magnesium block[3][7]. GluN2B-containing NMDA receptors are highly expressed in the forebrain and play critical roles in synaptic plasticity, learning, memory, and the modulation of synaptic strength[1][3][7]. These receptors are implicated in a variety of neuropsychiatric and neurodegenerative disorders, including Alzheimer’s disease, where altered GluN2B signaling may contribute to synaptic dysfunction and neuron loss[6]. Pharmacologically, GluN2B-selective antagonists (such as ifenprodil and Ro 25-6981) are being explored for their therapeutic potential in neurodegenerative, mood, and cognitive disorders[6][8]. The subunit is also referred to as NR2B or GRIN2B and is genetically encoded by the GRIN2B gene. Overactivation can lead to excitotoxicity and associated neuronal damage, making this subunit both a key signaling component and a therapeutic target, with safety concerns including potential cognitive deficits if NMDA signaling is overly inhibited[6].

Other names

NR2BGRIN2BGluRε2NMDA receptor subunit 2BGluN2B NMDA receptor

Antagonists inhibit Ca²⁺ influx by blocking channel activity; Negative allosteric modulators reduce receptor function; Some drugs bind selective allosteric sites on GluN2B subunit