Role of the excitotoxic mechanism in the development of neuronal damage following repeated brief cerebral ischemia in the gerbil: protective effects of MK-801 and pentobarbital.
Pretreatment with MK-801 (an NMDA antagonist) or pentobarbital (a GABAA receptor-effector) ameliorated histopathological neuronal damage to the hippocampal CA1 subfield and to the thalamus following three 2-min forebrain ischemia at 1-h intervals in the gerbil. Flunarizine, a calcium antagonist, failed to prevent the neuronal damage. The results suggest that the excitotoxic mechanism plays a role in the neuronal damage following repeated ischemia.
Kato
H
H
Department of Neurology, Tohoku University School of Medicine, Sendai, Japan.
Araki
T
T
Kogure
K
K
D000818:Animals; D003986:Dibenzocycloheptenes / Q000627:therapeutic use*; D016291:Dizocilpine Maleate; D005444:Flunarizine / Q000627:therapeutic use; D005849:Gerbillinae; D002546:Ischemic Attack, Transient / Q000188:drug therapy* / Q000473:pathology; D008297:Male; D010424:Pentobarbital / Q000627:therapeutic use*; D011963:Receptors, GABA-A / Q000187:drug effects / Q000502:physiology*; D016194:Receptors, N-Methyl-D-Aspartate; D017981:Receptors, Neurotransmitter / Q000037:antagonists & inhibitors / Q000502:physiology*
D003986:Dibenzocycloheptenes; D011963:Receptors, GABA-A; D016194:Receptors, N-Methyl-D-Aspartate; D017981:Receptors, Neurotransmitter; D016291:Dizocilpine Maleate; D010424:Pentobarbital; D005444:Flunarizine