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. 2020 Sep 16;42(6):861–870. doi: 10.1038/s41401-020-00521-3

Fig. 5. HDAC6 dysfunction mediates aberrant dendritic maturation in MSNs.

Fig. 5

a Immunofluorescence labeling of HDAC6 in GABA+ and TUJ1+ MSNs. Scale bar = 10 μm. b Cultured MSNs treated with various doses of ketamine or vehicle for 24 h were subjected to Western blotting with antibodies against total HDAC6, acetyl-α-tubulin and α-tubulin. β-Actin was used as an internal reference. c The expression of total HDAC6 and acetyl-α-tubulin was calculated (n = 3). d Quantitative real-time PCR (RT-PCR) analysis of HDAC6 expression in the 100 μM ketamine-treated and vehicle groups (n = 3). e Cultured MSNs treated with 50 or 100 μM ketamine or vehicle for 24 h were subjected to Western blotting with antibodies against HDAC6. α-Tubulin was used as a control for cytoplasmic proteins, while H3 was used as a control for nuclear proteins. The expression of HDAC6 in the cytoplasmic (f) and nuclear (g) fractions was calculated. h Schematic and timeline of the experiments. i Comparison of MSN morphology between the vehicle group, HDAC6 inhibitor (tubastatin A and ACY-1215)-treated groups, and ketamine (100 μM)-treated group. The concentrations of tubastatin A and ACY-1215 were 0.1 μM. Scale bar = 10 μm. j Comparison of MSN spines in each group. Scale bar = 5 μm. k Morphometric assessment of dendritic length, dendrite number, and dendritic spine density. The data are expressed as the mean ± SEM; ns not significant; *P < 0.05 vs. the vehicle group.