Transient ischemia causes a reduction of Mg2+ blockade of NMDA receptors.
After transient ischemia, synaptic activation of neurons in CA1 results in an abnormally long depolarization. This is due to the appearance of an NMDA component which results from a decrease in the normal voltage-dependent blockade by Mg2+. The reduction of NMDA channel blockade is likely the cause of the hyperexcitability which follows transient ischemia and the subsequent delayed neuronal cell death, resulting from entry of calcium through hyperactive NMDA channels.
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Wadsworth Center for Laboratories and Research, New York State Department of Health, Albany 12201-0509.
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D015763:2-Amino-5-phosphonovalerate / Q000494:pharmacology; D000818:Animals; D015220:Calcium Channels / Q000187:drug effects / Q000378:metabolism; D016923:Cell Death / Q000502:physiology; D004594:Electrophysiology; D005998:Glycine / Q000494:pharmacology; D002546:Ischemic Attack, Transient / Q000378:metabolism*; D008274:Magnesium / Q000494:pharmacology*; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects; D051381:Rats; D016194:Receptors, N-Methyl-D-Aspartate / Q000037:antagonists & inhibitors*
D015220:Calcium Channels; D016194:Receptors, N-Methyl-D-Aspartate; D015763:2-Amino-5-phosphonovalerate; D008274:Magnesium; D005998:Glycine