Figure 4.

APα-induced [Ca2+]i increases result from influx of extracellular calcium and are mediated by the L-type calcium channel. (A) Neurons (3–4 DIV) were exposed to 500 nM APα or vehicle control in Ca2+-free medium at the time-point indicated by the arrow. In the medium without calcium, APα showed no effect on intracellular calcium concentration. A representative graph of four independent experiments is shown (N = 36 neurons/condition/experiment). (B) La3+ diminished APα-induced [Ca2+]i rises. Neurons (3–4 DIV) were incubated with or without 10 μM La3+ (a calcium channel blocker) for 30 minutes prior to and continuously throughout imaging, and 500 nM APα or vehicle was added at the time-point indicated by the arrow. (B1) Representative graph of three different experiments (N = 36 neurons/condition/experiment). (B2) Bar graph represents the summary of [Ca2+]i rise in response to control, 10 μM La3+, 500 nM APα, and APα + La3+. Data are mean ± SEM, *p < 0.05 compared to APα treated neurons; N = 3 experiments with 36 neurons/condition/experiment. (C) Nifedipine blocked APα induced [Ca2+]i rises. Neurons were incubated with or without 10 μM nifedipine (an L-type calcium channel blocker) for 30 minutes prior to and continuously throughout imaging, and 250 nM APα or vehicle was added at the time-point indicated by the arrow. (C1) The graph is representative of three different experiments (N = 36 neurons/condition/experiment). (C2) The bar graph represents quantitative changes in [Ca2+]i in response to control, 10 μM nifedipine, APα, and APα + 10 μM nifedipine. Data are mean ± SEM (**p < 0.01 compared to APα treated neurons; N = 36 neurons/condition/experiment).

Wang and Brinton BMC Neuroscience 2008 9(Suppl 2):S11   doi:10.1186/1471-2202-9-S2-S11