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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.
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.
In some cases the level or exposure-time may be critical, with some substances only becoming neurotoxic in certain doses or time periods. Some of the most common naturally occurring brain toxins that lead to neurotoxicity as a result of long term drug use are amyloid beta (Aβ), glutamate, dopamine, and oxygen radicals.
Glutamate cannot cross the blood–brain barrier unassisted, but it is actively transported out of the nervous system by a high affinity transport system, which maintains its concentration in brain fluids at a fairly constant level. [4] Glutamate is synthesized in the central nervous system from glutamine as part of the glutamate–glutamine ...
These levels previously were called serum glutamate-pyruvate transaminase (SGPT) and serum glutamate-oxaloacetate transaminase (SGOT). Elevated levels are sensitive for liver injury, meaning that they are likely to be present if there is injury.
The glutamate hypothesis of schizophrenia models the subset of pathologic mechanisms of schizophrenia linked to glutamatergic signaling. The hypothesis was initially based on a set of clinical, neuropathological, and, later, genetic findings pointing at a hypofunction of glutamatergic signaling via NMDA receptors .
Alanine transaminase (ALT), also known as alanine aminotransferase (ALT or ALAT), formerly serum glutamate-pyruvate transaminase (GPT) or serum glutamic-pyruvic transaminase (SGPT), is a transaminase enzyme (EC 2.6.1.2) that was first characterized in the mid-1950s by Arthur Karmen and colleagues. [1]
Elevated levels of alpha-ketoisocaproate (α-KIC) result in a reduction in glutamate, glutamine, and GABA. Additionally, an influx of alpha-ketoisocaproic acid transported by a monocarboxylate transporter (MCT) across the blood–brain barrier, may deplete glutamate and glutamine in astrocytes , an important type of glial cell, through ...