Figure 2
From: Glucose deficit triggers tau pathology and synaptic dysfunction in a tauopathy mouse model
Glucose deprivation impairs synaptic function in the h-tau mice. (a) Input/output (I/O) curves and representative field excitatory postsynaptic potentials (fEPSPs) at increasing stimulus strengths (0–300 μA) are shown for CTR and 2-deoxyglucose (DG) treated h-tau mice at 10 months of age. (b) Mean fEPSP slopes as a function of interpulse interval between the first and second fEPSPs evoked at CA3–CA1 synapses in slices from the same mice at 20, 50, 100, 200, and 1000 milliseconds in the same animals. (c) fEPSP slopes were recorded for 2 h and expressed as the percentage of pretetanus baseline in the same mice. (d) Long-term potentiation (LTP) magnitudes expressed as the percentages of baseline for 0 to 10 min post-tetanus (***P<0.001). (e) For the same groups of mice, LTP magnitudes expressed as the percentages of baseline for 110 to 120 min post-tetanus (***P<0001). Values represent mean±s.e.m.
