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Glutamate receptor 2 (GluR2) is a subunit of the AMPA-type ionotropic glutamate receptor, encoded by the GRIA2 gene[3][1][8]. It functions as a ligand-gated cation channel mediating fast excitatory synaptic transmission in the central nervous system, primarily through sodium influx but modulated calcium permeability depending on RNA editing at the Q/R site[1][6][5]. The subunit is crucial for normal synaptic function, neuroplasticity, and influences cellular responses to injury and disease[4][8]. GluR2-containing AMPA receptors are calcium-impermeable and insensitive to polyamine block, unlike GluR2-lacking receptors which are permeable to calcium and sensitive to polyamines[5]. Dysregulation or mutation of GluR2 impacts neuronal survival, disease states such as Alzheimer's, and responses to ischemic injury[1][2][6]. Drugs and endogenous modulators, including CB1 receptor agonists/antagonists, glutamatergic agonists, and AMPAR antagonists, interact with the receptor to modulate its activity and contribute to therapeutic interventions in neurological diseases[2][3][5][8].
Ligand binding induces conformational change leading to opening of cation channel, allowing sodium and calcium influx Drugs and endogenous molecules modulate channel conductance, desensitization/resensitization, and calcium permeability RNA editing of GluR2 (Q/R site) regulates calcium permeability and is essential for normal receptor function
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