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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]
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 ...
Glutamate receptors and impaired regulation (in particular, those resulting in excessive glutamate levels) are also one cause of excitotoxicity (described above), which itself has been implicated or associated with a number of specific neurodegenerative conditions where neural cell death or degradation within the brain occurs over time. [42] [46]
Excessive glutamate release can overstimulate the brain and lead to excitotoxicity causing cell death resulting in seizures or strokes. [22] Excitotoxicity has been implicated in certain chronic diseases including ischemic stroke , epilepsy , amyotrophic lateral sclerosis , Alzheimer's disease , Huntington disease , and Parkinson's disease .
When disturbed, an accumulation of glutamate occurs as a result of a mutation in the glutamate transporters, which act like pumps to clear glutamate from the synapse. This causes glutamate concentration to be several times higher in the blood than in the brain; in turn, the body must act to maintain equilibrium between the two concentrations by ...
During brain ischemia, glutamate is released in excess from the presynaptic terminal, leading to the uncontrollable opening of the glutamate receptors, including the NMDA and AMPA receptors, which allows for an excessive influx of Ca 2+ into the intracellular environment. Purinergic and NMDA receptors activate the pannexin-1 channels, which ...
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.
Common examples of neurotoxins include lead, [7] ethanol (drinking alcohol), [8] glutamate, [9] nitric oxide, [10] botulinum toxin (e.g. Botox), [11] tetanus toxin, [12] and tetrodotoxin. [6] Some substances such as nitric oxide and glutamate are in fact essential for proper function of the body and only exert neurotoxic effects at excessive ...