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Glutamic acid signaling


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Glutamic acid signaling

Glutamic acid signaling

The amino acid Glutamic acid is recognized as the primary excitatoryneurotransmitter in the mammalian central nervous system [1].

Glutamic acid may exert its influence on the cells via glutamate receptor:NMDA receptor [2], Ionotropic glutamate receptors [3], [4], [5], Galpha(i)-specific metabotropicglutamate GPCRs [6], and Galpha(q)-specific metabotropic glutamateGPCRs [7], [8]. It may lead to depolarization of astrocytesand transmission of nerve impulses, glutamate-receptor-mediated calcium signaling,G-protein signaling and other effects [1].

Recent developments have shown that glutamate receptors are broadly expressed intissues other than the brain by cells that have not traditionally been associated withglutamate-mediated signaling [1]. For example, the proliferation of severaltumour cells is highly sensitive to glutamate receptor antagonists [9];insulin and glucagon release is stimulated via Ionotropic glutamate receptorsAMPA receptor and Kainate receptor [10], [11]; andNMDA receptors are present in osteoblasts and osteoclasts, where they affect boneformation [12].

The cellular uptake of Glutamic acid is coupled to the transport of sodium andpotassium. The stoichiometry of this process is such that the inward movement of oneglutamate, three sodium ions and one proton are coupled to the outward transport of onepotassium ion [13], [1]. Most important Glutamic acidtransporters in brain are Solute carrier family 1 members 1, 2 and 3 (SLC1A1/EAAT3, SLC1A2/EAAT2 and GLAST1/EAAT1 ) [1],[14].

Intracellular Glutamic acid participates in different cell processes (e.g.,synthesis of Gamma-aminobutyric acid ( GABA ), (L)-Glutamine, proteintranslation) [1].

The release of Glutamic acid from cell may be realized via Vesicular glutamatetransporters 2 and 3 ( SLC17A6 and SLC17A8 ) [15].