High frequency discharges of gerbil hippocampal CA1 neurons shortly after ischemia.
It has been postulated that the central neurotoxicity of glutamate participates in the pathogenesis of the ischemia-induced neuronal death and the process of the neuronal death is initiated by overexcitation or depolarization of postsynaptic neurons induced by increased extracellular glutamate during ischemia. In the present study, in order to know whether ischemic neurons show the overexcitation, we studied changes of CA1 neuronal discharges in gerbil hippocampus induced by transient forebrain ischemia (1-5 min) using an extracellular unit recording technique. CA1 neurons showed the high frequency discharges shortly after ischemic insult of 90 sec, however, these discharges did not induce neuronal death. Delayed neuronal death in the CA1 sector was observed in animals with 5-min ischemia which did not induce high frequency discharges. Neuronal depolarization with no spike discharge may persist during and shortly after 5-min ischemia and initiate the delayed neuronal death.
Mitani
A
A
Department of Physiology, University of Ehime, School of Medicine, Japan.
Imon
H
H
Kataoka
K
K
D000200:Action Potentials; D000818:Animals; D005849:Gerbillinae; D006624:Hippocampus / Q000503:physiopathology*; D002546:Ischemic Attack, Transient / Q000503:physiopathology*