Fig. 4: Mouse model of heart failure exhibits impaired long-term potentiation and diminished hippocampal glucose uptake. | Nature Neuroscience

Fig. 4: Mouse model of heart failure exhibits impaired long-term potentiation and diminished hippocampal glucose uptake.

From: Heart failure-induced cognitive dysfunction is mediated by intracellular Ca2+ leak through ryanodine receptor type 2

Fig. 4

a, Schematic representation of a hippocampal brain slice for LTP experiments and the positioning of the stimulating and recording electrodes. b, fEPSPs in hippocampal slices from each experimental group (SHAM (n = 13), MI (n = 12), MI + ARM036 (n = 12), MI + S107 (n = 11), MI + propranolol (n = 17) and MI + SD-208 (n = 16)). c, fEPSPs at 150 min in all the experimental groups. d, Basal neurotransmission (fEPSP slope), which remained unaltered between the different groups. e, Representative microPET images of FDG uptake (percentage of injected dose per gram (%ID/g)) in the mouse brains of different groups. f, Quantification of FDG uptake in the brains of mice from different experimental groups shown as a percentage of the FDG uptake in the SHAM mice (SHAM (n = 17), MI (n = 6), MI + ARM036 (n = 9), MI + S107 (n = 6), MI+ propranolol (n = 7) and MI + SD-208 (n = 6)). g, Quantification of 2-min dynamic microPET scans of MI (n = 4) and SHAM (n = 4) mice demonstrating similar brain blood flow FDG uptake in the brains of both groups of mice during the first 2 min after intravenous injection (%ID/g). hj, pH, PO2 and PCO2 blood levels in SHAM (n = 6) and MI (n = 7) mice. Individual values are shown with the mean ± s.e.m. One-way ANOVA and Tukey’s test post hoc correction for multiple comparisons, *P < 0.05, SHAM versus MI or MI + ARM036; #P < 0.05, MI versus MI + S107, MI + propranolol or MI + SD-208. A t-test was used in hj. Data are derived from biologically independent samples. All statistical tests were two sided.

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