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Aceglutamide (brand name Neuramina), or aceglutamide aluminium (brand name Glumal), also known as acetylglutamine, is a psychostimulant, nootropic, and antiulcer agent that is marketed in Spain and Japan.
The first compound studied was glycine which was hypothesized by Daniel Javitt after observation that people with phencyclidine(PCP)-induced psychosis were lacking in glutamate transmission. [1] (PCP is an NMDA receptor antagonist that blocks glutamate.) In giving glycine to people with PCP-induced psychosis a recovery rate was noted.
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 ...
Over-the-counter (OTC) medicines at FamilyDoctor.org, maintained by the American Academy of Family Physicians. Contains extensive information on over-the-counter drugs and their responsible use, including specific guidance on several drug classes in question-and-answer format and information on common drug interactions.
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 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]
[10] [11] By blocking sodium or calcium channels, antiepileptic drugs reduce the release of excitatory glutamate, whose release is considered to be elevated in epilepsy, but also that of GABA. [12] This is probably a side effect or even the actual mechanism of action for some antiepileptic drugs, since GABA can itself, directly or indirectly ...