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Fig. 2 | Molecular Neurodegeneration

Fig. 2

From: Reduced presynaptic vesicle stores mediate cellular and network plasticity defects in an early-stage mouse model of Alzheimer’s disease

Fig. 2

Impaired spontaneous and evoked presynaptic release properties in 3xTg-AD mice. Representative traces of sEPSPs from (a) NonTg (black) and (b) 3xTg-AD (gray) CA1 neurons at baseline, PTP, and E-LTP time-points. c Bar graphs show elevated averaged sEPSP frequency in 3xTg-AD (gray) neurons compared to NonTg (black) at baseline, and remains elevated during PTP and E-LTP. In NonTg neurons, sEPSP frequency is increased during PTP relative to its baseline, and returns to baseline during E-LTP. d sEPSP amplitude is not significantly different between NonTg and 3xTg-AD neurons at all time-points. Data are presented as Mean ± SEM; *p < 0.05 and **p < 0.01 represents significantly different from NonTg, **^p < 0.01 represents significantly different from pre-tetanus baseline. e Bar graphs show averaged paired pulse ratio (PPR) responses during baseline, PTP and E-LTP at 25 ms ISI (left) and 50 ms ISI (right) from NonTg (black, and patterned black) and 3xTg-AD neurons (gray and patterned gray). At the 50 ms ISI, the 3xTg-AD mice do not show the reduced PPR during PTP and E-LTP relative to baseline, as seen in the NonTg mice, suggesting that vesicle release probability is not further increased during these periods (NonTg n = 10 neurons/6 mice; 3xTg-AD n = 10 neurons/6 mice). Insets: Representative traces from NonTg (black) and 3xTg-AD (gray) at 25 ms and 50 ms. Data are presented as Mean ± SEM; *p < 0.05 and **p < 0.01 represent significantly different from pre-tetanus baseline

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