Glutamate is said to be a chief excitatory neurotransmitter in a mammal’s central nervous system. It seems to be a significant component for neuroplasticity, the synaptic communication between neurons. It also seems to be pretty significant to learning and memory. But in high concentrations, glutamate becomes toxic thus over-exciting the neurons. Glutamate-induced excitotoxicity is identified to intensify harm caused by brain injury, stroke and other neurodegenerative diseases.
In order to comprehend probable methods to decrease the harm of extreme glutamate, experts at Georgetown University Medical Center have illustrated how, when high concentrations of glutamate set off the metabotropic glutamate receptor 1, they grow to be defensive. This concentration of glutamate is believed to be usually toxic.
The study proposes that this glutamate-induced protection apparently takes place due to the connection of mGlu1 receptors with the intracellular protein β-arrestin, which supposedly results in a constant phosphorylation of mitogen-activated protein kinases, and shields cells from apoptotic death.
Andrew Emery, a PhD candidate in the Interdisciplinary Program in Neuroscience at GUMC, commented, “Studies about the signal transduction involved in mGlu1-mediated neuroprotection may enhance our understanding of the role that this glutamate receptor plays in brain injury.”
He further mentioned that such studies may contribute to rational drug design for potential therapeutic approaches to protect against excitotoxic brain damage following injury, stroke and neurodegenerative diseases.
The study was presented at the 39th annual meeting of the Society for Neuroscience.