T-Type Calcium Channels Are Required to Maintain Viability of Neural Progenitor Cells

Figures

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  Fig. 1.. Expression of T-type calcium channels in different neuronal cell types during different developmental periods. (A) mRNA expression of T-type calcium channel subtypes in NPCs, primary cortical neurons, and astrocytes. (B) Protein expression of CaV3.1 in neuronal cells or (C) in the cortex during the developmental period.

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  Fig. 2.. Inhibition of T-type calcium channels decreases NPC viability. (A) Table summarizing the function of channel blockers and their effects on NPC viability. (B–F) Results of MTT analysis 24 h after pharmacological blockade of T or L-type calcium channels using NNC55-0396 (B), mibefradil (C), ML218 (D), NiCl2 (E), and nifedipine (F), in NPCs. (G–H) MTT results from astrocytes (G) and neurons (H) 24 h after treatment with T-type calcium channel inhibitors (NNC55-0396 and mibefradil). Graphs represent the mean ± SEM. N=4–13, *p<0.05 and ***p<0.001.

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  Fig. 3.. Apoptotic cell death in NPCs by T-type calcium channel blockade. (A) Images of PI staining of NPCs after treatment with T-type calcium channel inhibitors (NNC55-0396 and Mibefradil). (B) Change in apoptotic cell marker proteins after NNC55-0396 and mibefradil treatment (N=5–8). Graphs represent the mean ± SEM. *p<0.05.

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  Fig. 4.. Inhibition of T-type calcium channels reduces AKT and GSK3β phosphorylation. (A) NNC55-0396 and mibefradil decrease AKT phosphorylation within 10 min of treatment. (B) NNC55-0396 and mibefradil decrease AKT and GSK3β phosphorylation in a concentration-dependent manner (N=3–5). (C) Phosphorylation of ERK, JNK, and p38 did not change 10 min after T-type calcium channel blockade (N=3). Graphs represent the mean ± SEM. *p<0.05, **p<0.01, and ***p<0.001.