Fig. 2.

PLCL1 is crucial in neuronal excitability and its dosage imbalance affects glutamatergic and GABAergic synapse development in vitro. A Decreased VGLUT1 and VGAT density caused by Plcl1 knockdown. Morphology of the VGLUT1 and VGAT density of neurons transfected with Plcl1 shRNA and control NC vector. The skeleton represents dendrite segments and dendritic spines. Scale bar, 5 μm. B Statistical analysis of the total dendrite length, branching number, spine density (per 10 μm), VGLUT1 density (red puncta number per 10 μm), and VGAT density (blue puncta number per 10 μm) between NC and shRNA groups. Forty neurons from three independent experiments were measured and counted. P-value is determined by unpaired t-test. ***P <0.001. C PLCL1-WT and mutant variants of PLCL1 rescues (res) the phenotype of decreased VGLUT1 and VGAT density caused by Plcl1 knockdown. The specific morphology of neurons in each condition expressing the indicated vectors. All neurons were co-labeled with VGLUT1, VGAT, and GFP. Scale bar, 5 μm. D Statistical results for the VGLUT1 density and VGAT density between each group. Approximately 30 cells from three independent experiments were randomly selected and counted. P-value was determined by one-way ANOVA. Error bars, ± SEM. *P <0.05; **P <0.01.