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Title: Electrophysiological changes of CA1 pyramidal neurons following transient forebrain ischemia: an in vivo intracellular recording and staining study.
Author: Xu ZC, Pulsinelli WA.
Journal: J Neurophysiol; 1996 Sep; 76(3):1689-97. PubMed ID: 8890285.
Abstract:
1. Electrophysiological changes of CA1 pyramidal neurons in rat hippocampus were studied before, during 5 min forebrain ischemia, and after reperfusion using in vivo intracellular recording and staining techniques. 2. membrane input resistance of CA1 neurons decreased from 25.98 +/- 7.24 M omega (mean +/- SD, n = 42) before ischemia to 16.33 +/- 6.50 M omega shortly after the onset of ischemia (n = 6, P < 0.01). The input resistance fell to zero during ischemic depolarization and quickly returned to 24.42 +/- 10.36 M omega (n = 11) within 2 h after reperfusion. 3. The time constant of CA1 neurons decreased from 11.49 +/- 5.45 ms (n = 36) to 3.09 +/- 1.66 ms (n = 6, P < 0.01) during ischemia. The time constant remained significantly less than preischemic levels within 2 h after reperfusion (5.40 +/- 2.60 ms, n = 13, P < 0.01) and gradually returned to preischemic levels 4-5 h after reperfusion. 4. The spike height decreased from 91 +/- 10.35 mV (n = 45) before ischemia to 82 +/- 8.00 mV (n = 9, P < 0.05) within 2 h after reperfusion and fully returned to preischemic level 2-5 h after reperfusion. The spike width increased from 1.14 +/- 0.22 ms (n = 45) before ischemia to 1.36 +/- 0.22 ms (n = 9, P < 0.05) within 2 h after reperfusion and remained at this level 4-5 h after reperfusion. 5. The spike threshold significantly increased from -54 +/- 3.93 mV (n = 45) before ischemia to -49 +/- 5.04 mV (n = 8, P < 0.01) within 2 h after reperfusion. The rheobase increased accordingly from 0.34 +/- 0.16 nA (n = 41) to 0.73 +/- 0.26 nA (n = 6, P < 0.01). The spike threshold returned to control levels 4-5 h after reperfusion, while the rheobase was still significantly higher than control levels (0.50 +/- 0.21 nA, n = 16, P < 0.01). 6. The frequency of repetitive firing evoked by depolarizing current pulses was suppressed within 2 h after reperfusion (n = 6, P < 0.01). The spike frequency increased slightly 2-5 h after reperfusion but was still significantly below the control levels (n = 12, P < 0.01). 7. Spontaneous synaptic activities ceased during ischemia and remained depressed shortly after reperfusion. Spontaneous firing rate was 0.47 +/- 0.81 spikes/s (n = 34) before ischemia. No spontaneous firing was detected within 2 h after reperfusion, and the firing rate gradually returned to preischemic levels 2-5 h after reperfusion (0.28 +/- 0.96 spikes/s, n = 15). Neuronal hyperactivity as indicated by an increased spontaneous firing rate was not observed up to 7 h after reperfusion. 8. Stimulation of the contralateral commissural pathway elicited excitatory postsynaptic potentials (EPSPs) minutes after reperfusion, whereas inhibitory postsynaptic potentials (IPSPs) did not appear until approximately 1 h after reperfusion. Within 2 h after reperfusion, the amplitudes of EPSPs slightly increased compared with those before ischemia, and the duration of EPSPs significantly increased from 18.00 +/- 3.08 ms (n = 5) before ischemia to 26.83 +/- 4.26 ms (n = 6, P < 0.01). The amplitude and duration of EPSPs returned to preischemic levels 4-5 h after reperfusion. 9. Results from the present study indicate that the input resistance and time constant of CA1 pyramidal neurons decrease during cerebral ischemia. After 5 min of forebrain ischemia, the spontaneous neuronal activities, evoked synaptic potentials and excitability of CA1 neurons are transiently suppressed after reperfusion. No hyperactivity was observed up to 7 h after reperfusion.

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