The NMDA receptor contributes to anoxic aglcemic induced irreversible inhibition of synaptic transmission

Present recovery of CA1 field EPSP amplitude following various anoxic aglycemic (AA) periods was examined in rat hippocampal slices superfused with MK-801 (0.1 μM, 1 μM, 10 μM) or Mg²⁺-free artificial cerebrospinal fluid. Slices treated with 0.1 μM MK-801 showed greater percent recuperation of EPSP amplitude following 3 min 30 s of AA (36±12%vs6 ±4% in controls). Higher concentrations of MK-801 resulted in a greater recovery of EPSP amplitudes in more than one time period of AA, with 10 μM MK-801 providing protection in up to 4 min 30 s AA. Percent recuperation of EPSP amplitude was smaller in Mg²⁺-free slices following 2 min (34±15%vs81±11% in controls) and 2 min 30 (25±14%vs77±10% in controls) of AA. These results that the activation of theN-methyl-d-aspartate (NMDA) receptor channel by contribute to irreversible AA induced synaptic failure in CA1.