Effects of Transient Forebrain Ischemia in Area CA1 of the Gerbil Hippocampus: An in Vitro Study
Lasting loss of function in the CNS after episodes of cerebral ischemia is caused by neuronal cell death (Brierly and Graham, 1984). Among neurons the most vulnerable to transient ischemia are the CA1b pyramidal cells in the hippocampus. The response of these neurons to oxygen deprivation is rather unusual. Following a short period of temporary recovery the signs of degeneration appear gradually, 2–4 days after the ischemic episode (Kirino, 1982, Crain et al., 1988). This phenomen is known as “delayed neuronal death” (Kirino, 1982, Pulsinelli et al., 1982). It is hoped that experimental study of its mechanism may help to devise therapeutical interventions that could arrest the degenerative process. The delayed cell degeneration has been attributed to secondary failure of the circulation by some investigators (Ames et al., 1968) and to a slow, intrinsic neuronal process by others (Simon et al., 1984; Rothman and Olney, 1987). Cells vary greatly in their susceptibility to such damage, and this variability could also be explained either by vascular or by intrinsic cellular differences.
KeywordsPyramidal Cell Excitatory Amino Acid Mongolian Gerbil Population Spike Transient Ischemia
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