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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 ...
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.
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]
Glutamate, one of the most common neurochemicals in the brain, is an excitatory neurotransmitter involved in many aspects of brain function, including learning and memory. [86] Based upon animal models, exercise appears to normalize the excessive levels of glutamate neurotransmission into the nucleus accumbens that occurs in drug addiction. [21]
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 ...
Normal platelets placed in plasma from people with bipolar disorder do not demonstrate elevated levels of intracellular calcium, indicating that dysfunction lies intracellularly. One possible mechanism is that elevated inositol triphosphate (IP3) caused by hyperactive neuronal calcium sensor 1 causes excessive calcium release. [31]
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]