Local Plasticity of Dendritic Excitability Can Be Autonomous of Synaptic Plasticity and Regulated by Activity-Based Phosphorylation of Kv4.2
Figure 3
Kv4.2 channels are responsible for DED and the process requires Ca2+ and MEK.
(A–D) Example current measurements before (black) and after stimulation (grey) showing that DED is blocked by HpTx (A) and TTX (B). Moreover DED does not happen in the absence of Ca2+ (C) and is blocked by MEK inhibitor U0126 (D). (E) Bar graph summarizing effect of different drugs. When no drugs are applied 13%±1.7% DED is observed. Application of TTX (1 uM), TEA (20 mM) and Stromatotoxin-II (100 nM) reduced the amount of DED to ∼3% while application of Hptx (100 mM) or U0126 (10 uM) or removal of calcium from external solution completely abolishes DED. The dendritic excitability was measured using 2 s pulses and the DED was quantified as a percentage change between the averaged peak current before and after stimulation. For each treatment significance of differences between the excitability before and after the stimulation was tested with two tailed heteroscedastic Student's t-test. Comparison between conditions was conducted by one-way ANOVA with Tukey post hoc test and showed no significant difference between control and APV (p = 0.08) and a statistically significant difference between control and all other conditions with p<0.001.