Abstract
Glutamate, the major excitatory neurotransmitter in the mammalian nervous system, is also suggested to be the primary mediator of neurodegeneration in several neuropathological conditions ranging from acute stroke and epilepsy to chronic disorders, e.g., Alzheimer’s disease and Huntington’s chorea (1–3). These neurotoxic effects of glutamate are thought to be mediated via the activation of N-methyl-D-aspartate (NMDA) subtypes of glutamate receptors. In the presence of excessive amounts of glutamate, the NMDA channel remains open and allows extracellular calcium to enter the cells (4). Increased intracellular free calcium in turn triggers a broad spectrum of metabolic and ionic events, which, if uncontrolled, result in irreversible neuronal injury and death (5). Therefore, it is important to develop strategies to block the excessive activation of NMDA receptors.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
