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Glutamatergic neurotransmission. Glutamic oxaloacetic transaminase (GOT) converts α-ketoglutarate to glutamate in mitochondria. Glutamate also forms from glutamine via mitochondrial glutaminase. Glutamate is transported into vesicles [6] by VGlut1 (or possibly other subtypes) for exocytotic release into the synapse. Synaptic glutamate activates four main types of receptors. AMPA [2], kainate [3], and NMDA [4] receptors are cation channels. Membrane depolarization in response to their activation causes neuronal excitation through cation influx. Metabotropic receptors (mGluR) [1,8] are coupled to G proteins and are expressed on pre- and postsynaptic membranes. In addition, some mGluRs reside outside of the synapse. Postsynaptic mGluR excitation in this example [1] results from preventing K+ efflux, but other mechanisms of excitation exist. Presynaptic mGluRs act to inhibit [8] glutamate (and other Source: Biochemical and Molecular Basis, Goldfrank's Toxicologic Emergencies, 10e neurotransmitter) release through modulating intracellular Ca2+ concentrations, as do presynaptic GABAB receptors in response to GABA binding [9]. Howland M, Lewin NA, Nelson LS, Goldfrank LR. influx Goldfrank's Emergencies, Available at: Figure 14–14Citation: providesHoffman a more RS, detailed illustration of the NMDA receptor. Excessive of Ca2+Toxicologic through NMDA receptors10e; (and2015 through some AMPA and http://mhmedical.com/ Accessed: August 03, 2017 2+ 2+ kainate receptors) causes neuronal damage and cell death. A Mg ion normally blocks the NMDA receptor channel to prevent Ca influx despite Copyright © 2017depolarization McGraw-Hill Education. All rights reserved glutamate binding. However, of the neuronal membrane by cation influx resulting from activation of any of the other receptor types causes 2+ Mg to dissociate from the NMDA receptor and to allow potentially damaging inward Ca2+ currents in response to glutamate binding. Glutamate