Cardiac Arrest Induces Ischemic Long-Term Potentiation of Hippocampal CA1 Neurons That Occludes Physiological Long-Term Potentiation

Figure 1

Lasting potentiation of miniature excitatory postsynaptic currents (mEPSCs) induced by cardiac arrest. (a) A representative trace from a sham control of whole-cell voltage clamp recording of mEPSC events recorded from CA1 neurons in acute brain slices. Events were detected with Clampfit software and are indicated with an asterisk. (b) CA/CPR produced a rightward shift in the cumulative frequency distribution of mEPSC amplitudes relative to shams. Events from sham (black, events) or CA/CPR (red, events) mice were pooled to generate histograms. (c) CA/CPR produced an increase in mean mEPSC amplitudes compared to sham. Mean mEPSC amplitude was calculated for each recording (sham: ; CA/CPR: ), and means for groups were compared using Student’s unpaired t-test ( indicates ). (d) CA/CPR did not alter synaptic density in CA1 neurons. No change in mean mEPSC frequency was observed between sham and CA/CPR mice. Mean mEPSC frequency was calculated for each recording (sham: ; CA/CPR: ), and means for groups were compared using Student’s unpaired t-test.

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