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Reference.org
Extrasynaptic NMDA receptor
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<p>Extrasynaptic NMDA receptors are glutamate-gated <a href="/facts/Neurotransmitter_receptor/6a6WnCwT">neurotransmitter receptors</a> that are localized to non-synaptic sites on the <a href="/facts/Neuron/G7CyTVdH">neuron</a>al <a href="/facts/Cell_membrane/vAXSD0DT">cell surface</a>. In contrast to synaptic NMDA receptors that promote <a href="/facts/Acquired_neuroprotection/BJUuS54j">acquired neuroprotection</a> and <a href="/facts/Synaptic_plasticity/rdVFxItN">synaptic plasticity</a>, extrasynaptic NMDA receptors are coupled to activation of death-signaling pathways. Extrasynaptic NMDA receptors are responsible for initiating <a href="/facts/Excitotoxicity/DKnHA79x">excitotoxicity</a> and have been implicated in the etiology of <a href="/facts/Neurodegeneration/HTDrVEqc">neurodegenerative diseases</a>, including <a href="/facts/Stroke/DwpjdzY0">stroke</a>, <a href="/facts/Huntington%2527s_disease/2P6yCoeK">Huntington’s disease</a>, <a href="/facts/Alzheimer%2527s_disease/w7Ad6tdg">Alzheimer’s disease</a>, and <a href="/facts/Amyotrophic_lateral_sclerosis/9fIXnNL4">amyotrophic lateral sclerosis</a> (ALS). </p><p>Extrasynaptic NMDA receptors form a death signaling complex with the transient receptor potential cation channel subfamily M member 4 (TRPM4). The NMDAR/TRPM4 complex is considered central to glutamate excitotoxicity. NMDAR/TRPM4 interaction interface inhibitors (also known as 'interface inhibitors') disrupt the NMDAR/TRPM4 complex thereby detoxifying extrasynaptic NMDA receptors. In mouse disease models, interface inhibitors protect against stroke induced brain damage and retinal ganglion cell degeneration. </p>