Skip to main content
. Author manuscript; available in PMC: 2010 Feb 12.
Published in final edited form as: Neuron. 2009 Feb 12;61(3):351–358. doi: 10.1016/j.neuron.2008.12.030

Figure 3. L-IPS Translocation Follows a Ca++ Spike and Requires Ca++ Influx, L-type Ca2+ Channel Activity, and CaMKII Activation.

Figure 3

(A) L-IPS translocation of CaMKII by glutamate plus glycine was inhibited by BAPTA-AM (10 μM) or the CaMKII inhibitor KN93 (0.5 μM) but not by inhibitors of Ca++ release from intracellular stores CICR (combinations of 2-amino-ethoxydiphenylborate (2-APB; 100 μM), ryanodine (10 μM), thapsigargin (1 μM), and cyclopiazonic acid (CPA; 20 μM)). One-way ANOVA revealed a significant difference between groups (F(3, 28) = 4.34, p<0.05). Dunnett’s post-hoc analyses show differences from ECS control for BAPTA-AM and KN93 (* = p<0.05). (B) Calcium imaging with fluo-4FF AM in ECS + TTX indicated that a typical local stimulation results in a rise in Ca++ spreading to the entire somatodendritic domain. In the subtraction image of 165 msec after stimulation minus pre-stimulation, white indicates Ca++ elevation. Note that the non-stimulated cell at right shows no Ca++ elevation. (C) Nifedipine (10 μM) did not block the effect of a 1-min bath application of glutamate (100 μM) and glycine (10 μM) to increase CaMKII clustering (t(13) = 1.12, p>0.1). (D) Nifedipine blocked L-IPS CaMKII translocation (t(19) = 3.11, **p<0.01). Scale bar B 20 μm; C,D 10 μm.