Fig. 7
Blockade of A2AR Ameliorated Synaptic Plasticity Impairment of abGCs in APP/PS1 Mice. A Whole-cell recording from young abGCs. The left panel shows the low magnification IR-DIC view, with the stimulating electrode placed in the molecular layer to target the perforant path axons originating from the entorhinal cortex. The example picture depicts an abGC recorded with 40 × DIC (middle) and fluorescent view (right). B-D Intrinsic properties of abGCs and mGCs. Resting potential, input resistance, and membrane capacitance were compared between the groups. AbGCs from APP/PS1 mice displayed a more mature phenotype, which was partially reversed by SCH58261 treatment. E Summary of experiments showing LTP recorded in mGCs and abGCs of WT mice. The bottom row represents representative EPSPs taken before (black) and 50 min (red) after LTP induction by a physiologically relevant TBS (arrow). Scale bar = 30 ms and 3 mV. F Summary of experiments showing LTP recorded from abGCs of WT mice, APP/PS1 mice, and SCH58261-treated APP/PS1 mice. G-H Histograms showing the average amplitude of EPSPs during the first 10 min (G) and the last 10 min (H) post-TBS. AbGCs exhibited enhanced synaptic plasticity compared to mGCs in WT mice. The LTP amplitude decreased in abGCs of APP/PS1 mice, while treatment with SCH58261 eliminated the genotype-specific effects. Data are presented as the mean ± SEM, n = 10 neurons per group, with each neuron from an individual animal, *p < 0.05, **p < 0.01, ***p < 0.001 by one-way ANOVA followed by Sidak's post-hoc test