Fig. 6: The effect of CLCN4 KD on human neurogenesis and reversal of the CLCN4 KD phenotype by risperidone. | Translational Psychiatry

Fig. 6: The effect of CLCN4 KD on human neurogenesis and reversal of the CLCN4 KD phenotype by risperidone.

From: Developmental deficits, synapse and dendritic abnormalities in a Clcn4 KO autism mice model: endophenotypic target for ASD

Fig. 6

a CLCN4 mRNA expression was increased upon neuronal differentiation. b Representative images of hESC-derived NPCs and neurons. SOX2 and NESTIN were used as NPC markers, and TUJ1 and MAP2 were used as neuron markers for immunocytochemistry. c Real-time PCR showed that CLCN4 mRNA levels were decreased by CLCN4 KD. d Representative images of control (Ctrl) and CLCN4 KD. The number of CLCN4-positive neurons decreased in CLCN4 KD compared to Ctrl (e) CLCN4 KD were immunostained with MAP2 (f) Sholl analysis showed that the neurite complexity of CLCN4 KD neurons was decreased. Risperidone treatment restored the neurite complexity of CLCN4 KD to normal levels. All data were analyzed by t-test or one-way ANOVA are presented as the mean ± SEM. (Ctrl vs. shCLCN4; *p < 0.05, **p < 0.01, ***p < 0.001).

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