· General description
· Activation process
· Physiological role
Type |
·
Ligand-gated voltage-dependent glutamate
receptor · Others: AMPA, kainate) |
Location |
· Spinal cord: especially dorsal horn 2° nociceptive afferents · Brain: especially hippocampus |
Structure |
· Transmembrane, tetrameric (in vivo) · 2 x NR1 subunits (obligatory) – binds glycine · 2 x NR2 subunits (modulatory) – binds glutamate · Central ion channel pore with Mg2+ plug |
Binding sites |
· Glutamate site (agonist) · Glycine site (coagonist) · Phencyclidine site (within the pore): ketamine, PCP (non-competitive antagonists) · N2O and Xe: site unknown (non-competitive antagonists) |
1.Priming |
· Activation of adjacent AMPA or NK-1 receptors · Partial depolarisation -> removal of Mg2+ plug |
2.Coactivation |
· Binding of glycine |
3.Activation |
· Binding of glutamate · Ion flux (Ca2+ influx > Na+ influx = K+ efflux) · Cell-dependent downstream effects |
Receptor |
· Non-competitive antagonist at PCP site · ↓Receptor activation |
Cellular effect |
· ↓Ca2+-mediated cell activation · ↓2nd messenger signalling · ↓Gene transcription |
Analgesic effect |
· ↓Receptor excitability = wind-up -> ↓hyperalgaesia, allodynia · ↓Synaptic reinforcement = long-term potentiation · ↓Acute somatic and neuropathic pain · ↓Opioid requirement · ↓Progression to chronic pain · Less utility once chronic pain established |
Other use |
· Dissociative general anaesthesia, including single agent use · Poorly understood effect on cell toxicity o ↓Ca2+ mediated excitotoxicity o ↑Neuronal damage in young rodents · ? Beneficial effect in depression |
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