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Glutamate: Brain 'Glu' May Lead to Sticky Situation

 

 

Glutamate is the major excitatory neurotransmitter in the mammalian brain, and is released into the synaptic cleft by most neurons when they send signals to other neurons in the brain. Glutamate exerts its actions by binding to several classes of glutamate receptors which leads to a complex network of downstream signaling events. Overall, glutamate and other neurotransmitter signaling events rely heavily on protein phosphorylation which fuels signal transduction cascades. The increasing availability of phosphospecific antibodies to components in transmitter networks is enabling researchers to define and map complex signaling pathways.

Glutamate signaling plays a pivotal role in many physiological functions including learning and remembering. However, the “glu” that binds is also a potent neurotoxin and is increasingly being implicated in the pathogenesis of neurological diseases including stroke, head trauma, epilepsy, AIDs, Hungtington’s, Parkinson’s and Alzheimer’s disease. For example, during stroke and following head trauma, neurons release massive amounts of glutamate onto nearby neurons which become overexcited, overloaded with calcium and undergo

 

Glutamate Signaling Proteins

apoptosis. Inhibiting neuronal cell death with glutamate receptor blockers is an emerging therapeutic strategy for managing glutamate-related diseases, and dozens of blockers are now in research or clinical studies. See below for our Glutamate-related products.


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Key Publications

1.
Platt SR. 2005. The role of glutamate in central nervous system health and disease- A review. The Veterinary Journal. Epub ahead of print; doi:10.1016/j.tvjl.2005.11.007. View Abstract  

2.
Hara MR and SH Snyder. 2006. Cell signaling and neuronal death. Annu. Rev. Pharmocol. Toxicol. Epub ahead of print. doi:10.1146/annurev.pharmtox.47.120505.105311. View Abstract

3.
Chen H-SV and SA Lipton. 2006. The chemical biology of clinically tolerated NMDA receptor antagonists.
J Neurochemistry.
97:1611-1626.
View Abstract

 
 

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