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https://www.pinnaclet.com/glutamate.html#:~:text=It%20has%20a%20linear%20range%20of%20at%20least,warrantied%20for%2021%20days%20from%20time%20of%20shipment.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4526718/
Glutamate is the predominant excitatory neurotransmitter in the adult mammalian brain; thus, much of past epilepsy research has attempted to understand the role of glutamate in seizures and epilepsy. Seizures induce elevations in extracellular glutamate, which then contribute to excitotoxic damage.
https://pubmed.ncbi.nlm.nih.gov/27885637/
Hence, manipulations of discrete glutamate-glutamine cycle components may represent novel approaches to treat the disease. The goal of his review is to discuss some of the glutamate-glutamine cycle components that are altered in epilepsy, particularly neurotransmitters and metabolites, enzymes, amino acid transporters, and glutamate receptors.
https://swansonhealthcenter.com/health-issues/epilepsy/
Excitotoxicity due to glutamate is associated with stroke, amyotrophic lateral sclerosis, lathyrism, autism, some forms of mental retardation, Alzheimer’s disease and epilepsy. 1,2 There are numerous glutamate receptors in all organs and tissues.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4640931/
In humans, Chamoun and colleagues demonstrated that this rise in extracellular glutamate, recorded from 24 hours after injury, lasts for as long as four days, and is directly proportional to posttraumatic mortality .
https://onlinelibrary.wiley.com/doi/pdf/10.1002/mrdd.1410010309
Epilepsy, a paroxysmal disorder characterized by abnormal neuronal discharges, is common in children. While the causes of epilepsy are many, the fundamental disorder is secondary to abnormal synchronous discharges of a network of neurons. Whether or not a seizure occurs in a child depends upon the balance between excitability and inhibition.
https://www.sciencedirect.com/science/article/pii/S0006295221004020
These studies described excitotoxic glutamate concentrations of 5.9 µM before a seizure, 17.6 μM during a seizure onset, and 11.7 µM up to 16.5 min following the termination of a seizure, i.e., 2, 6 and 4-fold increases compared to basal glutamate concentrations, respectively , .
https://elischolar.library.yale.edu/cgi/viewcontent.cgi?article=1469&context=ymtdl
resting, at least six hours from any intracranially recorded seizure activity, and 168 ± 81 hrs (mean ±. SDEV) before the stimulation study, to avoid the effects of acute probe implantation, anesthesia, ictal. activity, behavioral stimuli, or food intake [188-190]. Patients were on a combination of AEDs (Table 1).
https://www.d.umn.edu/biology/documents/Bauer1.pdf
hypothesis. First, glutamate released from neurons during an epileptic seizure accumulates in brain interstitial fluid (Holmes, 2002), and glutamate has been shown to increase P-glycoprotein expression in rat brain endothelial cells (Zhu and Liu, 2004). Second, enhanced glutamatergic signaling increases COX-2 (Strauss and Marini, 2002), which ...
https://www.pinnaclet.com/glutamate.html
It has a linear range of at least 50 uM. We have successfully demonstrated that the glutamate biosensor works in vivo and can provide continuous monitoring of brain glutamate concentration changes for up to 36 hours. This biosensor is warrantied for 21 days from time of shipment.
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