Fig. 5

Blockade of A_2AR Enhanced DG Network Inhibition and Inhibited Neuronal Hyperexcitability. A Typical paired pulses responses at 50 ms interpuls interval evoked by stimulation of MPP in slices from different groups mice in normal aCSF. Scale bar = 10 ms and 1 mV, n = 6 animals per group. B Paired-pulse inhibition (PPI) of the population spike was examined in different groups of mice at a stimulation intensity which evoked a population spike of 1.5–2 mV amplitude. The PPI curve of APP/PS1 mice was shifted towards weaker inhibition. Treatment with SCH58261 shifted the paired-pulse inhibition curve of APP/PS1 mice toward control level. C Paired-pulse inhibition curves were fitted to the Boltzmann function and a hypothetical interpulse interval (IPI), at which equal amplitude of the first and the second population spike would be detected, was determined and compared between groups. The IPI was significantly shortened in APP/PS1 group, as shown in the bar graph. Treatment of SCH58261 prolonged the IPI of APP/PS1 mice. D Representative field potentials recorded in the granule cell layer of DG in response to paired electrical stimulus applied to MPP in Mg²⁺- free aCSF. Scale bar = 20 ms and 1 mV, n = 10 animals per group. E–F The number of population spikes overriding the fEPSPs in pulse1 (P1, E) and pulse2 (P2, F). The number of both P1 and P2 were significantly increased in APP/PS1 mice compared to WT mice. Treatment of SCH58261 decrease population spike frequency of APP/PS1mice. Data are presented as the mean ± SEM, *p < 0.05, **p < 0.01 by one-way ANOVA followed by Sidak’s post-hoc test