Fig. 5: Risperidone restores protein expression and morphology in Clcn4 KO neuronal cultures. | Translational Psychiatry

Fig. 5: Risperidone restores protein expression and morphology in Clcn4 KO neuronal cultures.

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

Fig. 5

a Primary cortical neurons from Clcn4 KO pups were harvested and immune-stained with MAP2. b In Clcn4 deleted neurons, cell viability decreased by 50% compared to WT. Five and 10 µM risperidone restored the viability of neurons from Clcn4 KO in a dose-dependent manner. c The number of MAP2-positive neurons decreased in KO cortical neurons compared to WT but restored after risperidone treatment. d In Sholl analysis, the length of the dendrites of Clcn4 KO neurons, was significantly shorter compared to WT, but the length of the dendrites after risperidone treatment was restored to WT level. e Sholl analysis showed that the neurite complexity of Clcn4 KO neurons was decreased. Risperidone treatment restored the neurite complexity of Clcn4 KO neurons to normal levels. f SYNAPSIN 1 expression was not different between neuronal lysates from Clcn4 KO and those from WT mice at DIV7 and DIV14, but the phosphorylation of SYNAPSIN 1 at Ser9 and Ser549 was significantly reduced in neurons from Clcn4 KO at DIV14. g At DIV7, risperidone treatment increased SYNAPSIN 1 Ser9 phosphorylation in Clcn4 KO compared to untreated KO. Additionally, PSD95 expression, but not phosphorylation, was elevated in risperidone-treated KO compared to WT and untreated KO. All data were analyzed by t-test or one-way ANOVA are presented as the mean ± SEM. (*p < 0.05, **p < 0.01, ***p < 0.001).

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