Abstract
Glutamate is the major excitatory neurotransmitter in the central nervous system. Considerable evidence suggests that both ionotropic and metabotropic glutamate receptors are involved in pain hypersensitivity. However, glutamate receptor-based therapies are limited by side-effects because the activities of glutamate receptors are essential for many important physiological functions. Here, we review recent key findings in molecular and cellular mechanisms of glutamate receptor regulation and their roles in triggering and sustaining pain hypersensitivity. Targeting these molecular mechanisms could form the basis for new therapeutic strategies for the treatment of chronic pain.
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.
