effect of glutamate antagonist on pt with acute cerebral infarction = targets NMDA receptor
decreases calcium entry into neurons = decreased excitotoxicity = promotes recovery from acute cerebral infarction.
This one was tricky but I think you couldโve done this one without knowledge of NMDA receptors. Stem told you that glutamate activates both non-NMDA and NMDA receptors but it activated only non-NMDA receptors in the early phase. That means NMDA receptors activate after non-NMDA receptors. That means something was delaying NMDA receptor activating and the only answer that made sense as the Mg inhibiting NMDA at resting potential. Once the cell is depolarized by non-NMDA receptors, NMDA receptors can be activated.
At resting membrane potential the NMDA receptors are blocked by Mg2+. The voltage dependent Mg2+ block is relieved upon depolarization of the post-synpatic membrane . The ligand dependent activation of the NMDA receptor requires co-activation by two ligands, namely glutamate and glycine.
An important related clinical application is remembering: Ovarian teratoma and their associations with: Anti-NMDA receptor encephalitis. This presents as: Psychiatric disturbance, memory deficits, seizures, dyskinesias, autonomic instability, language dysfunction.
FA: 2020; pg 228
don't forget about the Mg block! . . . . . .
submitted by โniboonsh(409)
https://www.youtube.com/watch?v=4-DuvwoH2zQ if ur lazy like me, this is a good refresher video