Responses of CA1 pyramidal neurons in rat hippocampus to transient forebrain ischemia: an in vivo intracellular recording study.
The electrophysiological responses of CA1 pyramidal neurons to 5 min forebrain ischemia were studied with intracellular recording and staining techniques in vivo. The baseline membrane potential rapidly depolarized to approximately -20 mV about 3 min after the onset of ischemia and began to repolarize 1-3 min after recirculation. The amplitude of this ischemic depolarization (ID) was related directly to the severity of ischemia and its latency of onset was inversely related to brain temperature. Spontaneous synaptic activity ceased shortly after ischemia onset while the evoke synaptic potentials lasted until shortly before the onset of ID. Inhibitory postsynaptic potentials (IPSPs) disappeared earlier than excitatory postsynaptic potentials (EPSPs) and the membrane input resistance of CA1 neurons increased after the onset of ischemia.
Xu
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ZC
Department of Neurology, College of Medicine, University of Tennessee, Memphis 38163.
Pulsinelli
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WA
D000200:Action Potentials / Q000502:physiology; D000818:Animals; D001831:Body Temperature / Q000502:physiology; D006624:Hippocampus / Q000473:pathology*; D002546:Ischemic Attack, Transient / Q000473:pathology*; D008297:Male; D008564:Membrane Potentials / Q000502:physiology; D010101:Oxygen Consumption / Q000502:physiology; D017966:Pyramidal Cells / Q000502:physiology*; D051381:Rats; D017208:Rats, Wistar; D013569:Synapses / Q000502:physiology