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. Author manuscript; available in PMC: 2010 Jul 1.
Published in final edited form as: Cell Calcium. 2009 May 2;46(1):30–38. doi: 10.1016/j.ceca.2009.03.018

Figure 4.

Figure 4

A. Depolarization-induced [Ca2+]i-elevation and its modulation by ryanodine (traces are shown as mean ± SEM). Inset shows Fluo-3 images before (1) and after (2) KCl puff. Calibration bar: 15 μm. B1. Depolarization-induced [Ca2+]i-elevation in the presence of kynurenic acid, nimodipine, and ryanodine. B2. Responses to caffeine in the control ACSF and the thapsigargin (TG)-containing ACSF in neurons. B3. The same neurons in B2 generated a [Ca2+]i-increase in response to KCl-induced depolarization. A caffeine-puff of 5s immediately before the depolarization (indicated by a horizontal bar) amplified a peak amplitude of the [Ca2+]i-increase. On the other hand, TG reduced the [Ca2+]i-peak to less than 1/3 of the control. C1. Depolarization-induced [Ca2+]i-elevation in the control ACSF and its reduction by nimodipine and ryanodine. C2. Effect of ω-conotoxin on depolarization-induced [Ca2+]i-elevation. C3. Effect of ω-agatoxin on depolarization-induced [Ca2+]i-elevation. D. Time-dependent changes in depolarization-induced [Ca2+]i-elevation in control, nimodipine, and ryanodine. E1. Changes in peak amplitude and peak latency of depolarization-induced [Ca2+]i-elevation by ryanodine and nimodipine. Inset shows differences in peak [Ca2+]i-elevation and the peak latency between control and nimodipine (green) and between nimodipine and nimodipine plus ryanodine (black). E2. Changes in the identical parameters shown in E1 in the presence of kynurenic acid in ACSF.