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

Figure 2

Increased AMPA receptor phosphorylation after CA/CPR. (a) Representative blots of protein expression from synaptic fractions of sham and CA/CPR hippocampus. Blots were cropped to show bands at molecular weight for indicated proteins. (b) Normalized phosphorylated S831: total GluR1 expression was calculated for each sample by dividing optical density of phosphoS831 by total GluR1 density within the same blot. (c) Normalized GluR1 expression was calculated for each sample by dividing optical density of total GluR1 by β-actin density within the same blot. (d) Normalized GluR2/3 expression was calculated for each sample by dividing optical density of total GluR2/3 by β-actin density within the same blot. (e) Normalized GluN1 expression was calculated for each sample by dividing optical density of total GluN1 by β-actin density within the same blot. (f) Normalized PSD-95 expression was calculated for each sample by dividing optical density of PSD-95 by β-actin density within the same blot. Values were normalized to sham controls. Shams () and CA/CPR () groups were compared using Student’s t-test. indicates .

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