Skip to main content
. Author manuscript; available in PMC: 2017 Sep 5.
Published in final edited form as: Cell Rep. 2017 Aug 8;20(6):1335–1347. doi: 10.1016/j.celrep.2017.07.030

Figure 4. Acetylation regulates AMPAR trafficking, turnover and accumulation in neuron.

Figure 4

(A–D) In cultured hippocampal neurons, inhibition of SIRT2 activity by B2 (20 μM, 24 hrs) resulted in a suppression in internalization (A, n ≥ 15 cells/group), an increase in surface expression (A, B, n ≥ 15 cells/group) and an elevated cellular accumulation of AMPARs (C, n ≥ 15 cells/group), as well as an increase in AMPAR-mediated synaptic transmission (D, n = 8 cells/group), without affecting the insertion of AMPARs (B, n ≥ 15 cells/group) or the density of AMPAR puncta (C, n ≥ 15 cells/group). Scale bar, 20 μm (A, B), 5 μm (C). (E) In HEK cells expressing GluA1 with pcDNA control, or GluA1 with SIRT2, cycloheximide (CHX) tracing showed faster degradation of GluA1 in cells co-expressing SIRT2 (lower panel) (n = 3). Bar graphs represent mean ± S.E., ＊P < 0.05, ＊＊P < 0.01, ＊＊＊P < 0.001, NS, not significant. Student’s two-tailed t test.