Fig. 8

Parkin mutation/knockdown impairs the induction of LTD. a Representative images of surface GluA1 staining (red) in 14–16 DIV hippocampal neurons expressing GFP, shParkin or shParkin-WT, under the control condition (no treatment) or after chemical LTP (cLTP) induction. Scale bar, 10 μm. b Quantification of the ratio of GluA1 intensity after cLTP induction to the control condition for neurons expressing GFP, shParkin, or shParkin-WT. c Same as (a), but for control condition or chemical LTD (cLTD) induction. Scale bar, 10 μm. d Quantification of the ratio of GluA1 intensity after cLTD induction to the control condition for neurons expressing GFP, shParkin, or shParkin-WT. e Representative images of surface GluA1 staining (red) in 14–16 DIV hippocampal neurons expressing GFP, shParkin or shParkin-WT/-T240M/-R275W/-R334C/-G430D constructs, under the control condition or after cLTD induction. Scale bar, 10 μm. f Quantification of the ratio of GluA1 intensity after cLTD induction to the control condition for neurons expressing GFP, shParkin or shParkin-WT/-T240M/-R275W/-R334C/-G430D constructs. For panels (b) and (d), n ≥ 50 fields of view per condition with > 100 GluA1 puncta per field, results confirmed in 3 independent experiments. ***P < 0.001, unpaired t test. For panel (f), n ≥ 40 fields of view per condition with > 100 GluA1 puncta per field, results confirmed in 3 independent experiments. ***P < 0.001, one-way ANOVA, error bars represent SEM