MK-801, but not anisomycin, inhibits the induction of tolerance to ischemia in the gerbil hippocampus.
We examined whether MK-801, an N-methyl-D-aspartate (NMDA)-receptor antagonist, or anisomycin, a reversible protein synthesis inhibitor, inhibits the induction of ischemic tolerance following preconditioning with sublethal ischemia in gerbil hippocampus. Preconditioning with 2 min of ischemia, which induced heat shock protein-72 immunoreactivity, prevented hippocampal CA1 neuronal damage following 3 min of ischemia produced 3 days later. MK-801, but not anisomycin, inhibited the induction of tolerance although the heat shock protein synthesis was reduced in both groups. The present result suggests that NMDA receptor activation, causing stress response, induces the ischemic tolerance.
Kato
H
H
Department of Neurology, Tohoku University School of Medicine, Sendai, Japan.
Liu
Y
Y
Araki
T
T
Kogure
K
K
D000818:Animals; D000841:Anisomycin / Q000494:pharmacology*; D001831:Body Temperature / Q000187:drug effects; D002545:Brain Ischemia / Q000473:pathology*; D016291:Dizocilpine Maleate / Q000494:pharmacology*; D004569:Electroencephalography; D005849:Gerbillinae; D006624:Hippocampus / Q000098:blood supply* / Q000187:drug effects / Q000473:pathology; D007150:Immunohistochemistry; D008297:Male; D016194:Receptors, N-Methyl-D-Aspartate / Q000187:drug effects
D016194:Receptors, N-Methyl-D-Aspartate; D000841:Anisomycin; D016291:Dizocilpine Maleate