Fig. 6: ZDHHC8 interacts with GluA1 and regulates GluA1 trafficking to the neuronal surface in the hippocampus.
From: ZDHHC8 critically regulates seizure susceptibility in epilepsy

a–d Immunoprecipitation of KA-induced epileptic mice hippocampal lysates. ZDHHC8 co-immunoprecipitates with GluA1 (a), GluA2 (b), GluA3 (c), and GluA 4 (d). ZDHHC8 was mainly bound to GluA1 (a). e–h Western blot analysis of the cell expression of GluA1 in hippocampal tissues from rAAV-ZDHHC8-sh, rAAV-Scr-sh, Control, rAAV-Empty-GFP, and rAAV-ZDHHC8 mice in the KA- (e, f) and pilocarpine-induced (g, h) chronic seizure models. f(a), f(b); h(a), h(b) Bar graph showing that the amount of cell-surface GluA1 decreased significantly in rAAV-ZDHHC8-sh tissues and increased in rAAV-ZDHHC8-overexpressing tissues, whereas that of GABAA β2/3 was unchanged. f(c); h(c) Intracellular GluA1 expression behaved opposite to that of GluA1 cell-surface expression. The levels were normalized to the total protein for each receptor. Error bars indicate the mean ± SEM, n = 5 independent experiments for each group, *P < 0.05, **P < 0.01, and ***P < 0.001; one-way ANOVA