Depolarization promotes GAD 65-mediated GABA synthesis by a post-translational mechanism in neural stem cell-derived neurons
Article first published online: 11 JAN 2008
European Journal of Neuroscience
Volume 27, Issue 2, pages 269–283, January 2008
How to Cite
Gakhar-Koppole, N., Bengtson, C. P., Parlato, R., Horsch, K., Eckstein, V. and Ciccolini, F. (2008), Depolarization promotes GAD 65-mediated GABA synthesis by a post-translational mechanism in neural stem cell-derived neurons. European Journal of Neuroscience, 27: 269–283. doi: 10.1111/j.1460-9568.2007.06020.x
- Issue published online: 18 JAN 2008
- Article first published online: 11 JAN 2008
- Received 1 June 2007, revised 1 November 2007, accepted 27 November 2007
Fig. S1. A merge of DIC image and immunostaining for Tuj1 identifying neurons in differentiating striatal NPC culture on DAP 1.
Fig. S2. Calcium influx in response to acute high K+ differentiation (HiK) application in neurons that were kept in normal differentiation medium, or treated with for 3–6 h prior to HiK application with nifedipine, ω-conotoxin MVIIC, and mibefradil dihydrochloride.
Fig. S3. Percentages of neurons that were GABA-immunopositive in striatal NPC cultures that were exposed to differentiation medium or high K+ differentiation (HiK) on DAP 1 for 24 h in the presence or absence of bicuculline; GABA; glutamate; an activator of TRP channels, OAG; and the GAT 1 inhibitor, SKF 89976A hydrochloride.
Video S1. A Ca2+ recording.
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