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Postischemic alterations of complex spike cell discharges and evoked potentials in rat hippocampal CA1 region
Author(s) -
Furukawa K.,
Yamana K.,
Kogure K.
Publication year - 1992
Publication title -
acta neurologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.967
H-Index - 95
eISSN - 1600-0404
pISSN - 0001-6314
DOI - 10.1111/j.1600-0404.1992.tb05056.x
Subject(s) - ischemia , hippocampal formation , neurotransmission , medicine , electrophysiology , anesthesia , endocrinology , hippocampus , chemistry , receptor
Postischemic alterations of spontaneous discharges of complex spike cells (CS cells) and evoked potential in the rat hippocampal CA1 region were studied. Following 5 min of ischemia, CS cell discharge reappeared approximately 5 min after reperfusion and the frequency remained low, reaching a final value of 66.1 ± 16.0% (n = 11) of preischemic frequency 2 h later. However, only one of 7 CS cells subjected to 20 min of ischemia exhibited discharges 2 h later. In the group with 5 min of ischemia, we obtained CS cell discharges from all rats at both 1 and 2 days after ischemia, with cluster frequencies indistinguishable from preischemic levels. In the group with 20 min of ischemia, discharges were noted in 7 neurons of 11 rats after 1 day, and in only 2 neurons of 8 rats after 2 days: their mean frequencies were lower than preischemic levels. In experiments of evoked potentials, the mean percentages of amplitudes of the post‐synaptic potential (psp) 2 h after 3, 5 and 20 min of ischemia were 98.0 ± 10.7 (n = 8), 70.7 ± 8.22 (n = 9) and 45.1 ± 6.34% (n = 7) of preischemic amplitudes, respectively. These results suggest that the functional deterioration of spike generation, as well as synaptic transmission, starts during transient ischemia and/or at the early stage of reperfusion.