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Glutamate is a very major constituent of a wide variety of proteins; consequently it is one of the most abundant amino acids in the human body. [1] Glutamate is formally classified as a non-essential amino acid, because it can be synthesized (in sufficient quantities for health) from α-ketoglutaric acid, which is produced as part of the citric acid cycle by a series of reactions whose ...
Glutamatergic means "related to glutamate". A glutamatergic agent (or drug ) is a chemical that directly modulates the excitatory amino acid ( glutamate / aspartate ) system in the body or brain. Examples include excitatory amino acid receptor agonists , excitatory amino acid receptor antagonists , and excitatory amino acid reuptake inhibitors .
NMDA receptors are glutamate-gated cation channels that allow for an increase of calcium permeability. Channel activation of NMDA receptors is a result of the binding of two co agonists, glycine and glutamate. Overactivation of NMDA receptors, causing excessive influx of Ca 2+ can lead to excitotoxicity. Excitotoxicity is implied to be involved ...
These glutamate receptors are suggested to play a role in modulating gene expression in glial cells, both during the proliferation and differentiation of glial precursor cells in brain development and in mature glial cells. [12] Glutamate receptors serve to facilitate the impact of the neurotransmitter glutamate in the central nervous system.
GLP-1 drugs may protect the brain from inflammation, some studies say, but others warn they may increase depression risk. Image credit: James Manning – PA Images/Getty Images.
Excessive glutamate release is a known major cause of neuronal cell death. Glutamate causes neurotoxicity due to excitotoxicity and oxidative glutamate toxicity. Evidence from animal studies suggests that some people may be more genetically sensitive to the neurotoxic and brain damage associated with binge drinking regimes.
Glutamate is a prime example of an excitotoxin in the brain, and it is also the major excitatory neurotransmitter in the central nervous system of mammals. [14] During normal conditions, glutamate concentration can be increased up to 1mM in the synaptic cleft, which is rapidly decreased in the lapse of milliseconds. [15]
In the event of a mutation, the glutamate transporters are unable to pump the glutamate back into the cells; thus a higher concentration accumulates at the glutamate receptors. This opens the ion channels, allowing calcium to enter the cell causing excitotoxicity.