Fig. 5
From: Modifying Rap1-signalling by targeting Pde6δ is neuroprotective in models of Alzheimer’s disease
REM represses VGCC activity in primary hippocampal neuron cultures. a Quantification of [Ca2+]i influx using Ca2+ indicator Fura-2 after KCl instigated depolarisation at increasing concentrations in function of 1.5 μM REM treatment. Graphs represent the normalised mean Area’s Under the Curve’s (AUC) over a 4 min period after the addition of KCl (n = 3; Treatment: P = 0.0015; DF = 1; F (1, 20)=13.47; KCl concentration: P < 0.0001; DF = 4; F (4, 20)= 68.45; Multiple comparisons test: 45 mM KCl Vehicle/REM: P = 0.0454; t = 2.881; DF = 20). b AUC’s are determined as in (a) after exposure to 45 mM KCl in presence or absence of 12.5 μM nifedipine as indicated. A representative Ca2+ trace (+/−REM) is depicted in the small inset next to the graph. (n = 5; REM Treatment: P = 0.0003; DF = 1; F (1, 16)=20.87; +/− Nifedipine: P < 0.0001; DF = 1; F (1, 16)=60.32; Interaction: P = 0.008; DF = 1; F(1.16) = 9.156; Multiple comparisons test: Vehicle/REM – nifedipine: P = 0.0004; t = 5.37; DF = 16; Vehicle +/− nifedipine: P < 0.0001; t = 7.631; DF = 16; REM +/− nifedipine: P = 0.0241; t = 3.352; DF = 16)