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Journal of Neuroscience, Vol 9, 3966-3975, Copyright © 1989 by Society for Neuroscience
Postischemic synaptic physiology in area CA1 of the gerbil hippocampus studied in vitro
L Urban, KH Neill, BJ Crain, JV Nadler and GG Somjen
Department of Cell Biology, Duke University Medical Center, Durham, North Carolina 27710.
After transient forebrain ischemia in the Mongolian gerbil, CA1b
hippocampal pyramidal cells degenerate during a period of 2-4 d. We tested
the hypothesis that this delayed neuronal death is preceded by excessive
synaptic excitation. Hippocampal slices were prepared from gerbils that had
been subjected to a 5 min occlusion of both common carotid arteries.
Input/output curves demonstrated enhancement of the initial slope of the
Schaffer collateral-commissural focally recorded EPSP at all stimulus
currents between 5 and 10 hr after the ischemic insult. The duration of the
focally recorded EPSP also increased. At the same time, the excitability of
the CA1b pyramidal cells decreased. Thus, the EPSP brought fewer pyramidal
cells to threshold than the same size EPSP in control slices. During the
first 14 hr after ischemia, the antidromic population spike remained
unaffected. By 24 hr after ischemia, however, the focally recorded EPSP and
both orthodromic and antidromic population spikes were markedly depressed,
and they declined further over the next 2 d. No recovery was detected. In
the same slices, transient ischemia only mildly and reversibly affected the
response of dentate granule cells to perforant path stimulation and did not
affect their response to antidromic stimulation. Hippocampal slices
adjacent to those used for electrophysiological recording were analyzed
histologically. Examination of somatic argyrophilia confirmed that CA1b
pyramidal cells suffered delayed neuronal death, whereas dentate granule
cells remained intact. Pyramidal cell argyrophilia was, however, not
detected until 2 d after these neurons had become virtually inexcitable. We
conclude that CA1b pyramidal cells begin to lose electrophysiological
function well before definite morphological signs of degeneration become
visible. The observation of enhanced excitatory transmission 5-10 hr after
reperfusion is consistent with the idea that delayed ischemic neuronal
death results, at least in part, from excessive excitation.
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