TY - JOUR
T1 - Postischemic alterations of complex spike cell discharges and evoked potentials in rat hippocampal CA1 region
AU - Furukawa, K.
AU - Yamana, K.
AU - Kogure, K.
PY - 1992/8
Y1 - 1992/8
N2 - 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. 1992 Blackwell Munksgaard
AB - 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. 1992 Blackwell Munksgaard
KW - complex spike cell
KW - delayed neuronal death
KW - evoked potential
KW - hippocampus
KW - ischemia
KW - rat
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U2 - 10.1111/j.1600-0404.1992.tb05056.x
DO - 10.1111/j.1600-0404.1992.tb05056.x
M3 - Article
C2 - 1329428
AN - SCOPUS:0026655771
VL - 86
SP - 142
EP - 147
JO - Acta Neurologica Scandinavica
JF - Acta Neurologica Scandinavica
SN - 0001-6314
IS - 2
ER -