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For example, when glutamate receptors such as the NMDA receptor or AMPA receptor encounter excessive levels of the excitatory neurotransmitter, glutamate, significant neuronal damage might ensue. Excess glutamate allows high levels of calcium ions (Ca 2+) to enter the cell.
Among its many physiological effects that may play a role in depression, ketamine raises levels of glutamate, which may be how it offers such immediate relief from depression. Some people feel ...
[162] [163] This network is involved in high level cognitive functions such as maintaining and using information in working memory, problem solving, and decision making. [ 161 ] [ 164 ] Deficiencies in this network are common in most major psychiatric and neurological disorders, including depression.
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]
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 ...
With the loss of AMPA receptors, the postsynaptic Purkinje cell response to glutamate release from parallel fibers is depressed. [2] Calcium triggering in the cerebellum is a critical mechanism involved in long-term depression. Parallel fibre terminals and climbing fibres work together in a positive feedback loop for invoking high calcium ...
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.
In 1999, Moghaddam and her colleagues tested the compound LY354740, a metabotropic glutamate receptor agonist, which they found to suppress aberrant glutamate release, reduced behavioral disruptions in animals given PCP, and overall have less side effects than typical benzodiazepines used to treat certain symptoms of schizophrenia. [1]