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. 2010 Sep 23;5(9):e12908. doi: 10.1371/journal.pone.0012908

Figure 3. HDAC6 activity inhibition reduces the rate of axon elongation.

Figure 3

(A) α-tubulin acetylation in 2 DIV hippocampal neurons treated with the HDAC6 specific inhibitor tubacin, its non-active analog, niltubacin, or its vehicle, DMSO (control). The graph represents the mean ± SEM of the acetylated-α-tubulin/α-tubulin ratio normalized to control in 3 independent experiments. ****p<0.0001, paired t-test. (B) 2 DIV hippocampal neurons cultured in the presence of vehicle (DMSO), the HDAC6 inhibitor (tubacin, 10 µM) and its inactive compound (niltubacin, 10 µM). Neurons were stained for MAP2 and tau-1. Scale bar  = 100 µm. The graph represents the percentage of neurons with a tau-1 positive process. Data represent the mean ± SEM of 3 independent experiments (500 neurons/experimental condition and experiment). ***p<0.001, paired t-test. (C) 4 DIV hippocampal neurons cultured from 48 hours to 4 days in vitro in the presence of DMSO, tubacin (10 µM) or niltubacin (10 µM), and stained as indicated in (B). Scale bar  = 100 µm. The graph represents the axonal length of control neurons fixed at 2 DIV or 4 DIV, and of 4 DIV neurons treated from 2 DIV to 4 DIV with tubacin or niltubacin. Data represent the mean ± SEM of 3 independent experiments (150 neurons/experimental condition and experiment). **p<0.01, paired t-test.