Abstract
Epilepsy is one of the most common neurological disorders characterized by recurrent seizures. The mechanism of epilepsy remains unclear and previous studies suggest that N-methyl-D-aspartate receptors (NMDARs) play an important role in abnormal discharges, nerve conduction, neuron injury and inflammation, thereby they may participate in epileptogenesis. NMDARs belong to a family of ionotropic glutamate receptors that play essential roles in excitatory neurotransmission and synaptic plasticity in the mammalian CNS. Despite numerous studies focusing on the role of NMDAR in epilepsy, the relationship appeared to be elusive. In this article, we reviewed the regulation of NMDAR and possible mechanisms of NMDAR in epilepsy and in respect of onset, development, and treatment, trying to provide more evidence for future studies.
Highlights
Epilepsy is one of the most common neurological disorders characterized by recurrent seizures
Related studies have shown that the epileptogenesis of pilocarpineinduced medial temporal lobe epilepsy (MTLE) is associated with abnormal regulation of N-methyl-D-aspartate receptors (NMDARs)-mediated excitatory neuronal mechanisms and neuronal activity regulated by Ca2+/CaMK signaling (Canto et al, 2021)
cAMP response elementbinding protein (CREB)-dependent gene expression, which is closely associated with neuroprotection against apoptosis and excitatory damage, so the study of the regulatory mechanism of the NMDAR-CREB pathway in epilepsy is conducive to the neuroprotection of the epileptic brain
Summary
Epilepsy is one of the most common neurological disorders characterized by recurrent seizures. NMDAR can promote activation of calpain and LMP, while inhibition of calpain and LMP may be an effective method to reduce neuronal death caused by NMDAR-mediated excitotoxicity in epilepsy. Inhibition of PARP-dependent cell death pathways has been shown to prevent seizure-induced neuronal damage (D’Orsi et al, 2016).
Sign-in/Register to view highlights & summary 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.
