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January 2020

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Increased expression of schizophrenia-associated gene C4 leads to hypoconnectivity of prefrontal cortex and reduced social interaction
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Schizophrenia is a severe mental disorder with an unclear pathophysiology. Increased expression of the immune gene, which encodes complement C4, has been linked to a greater risk of developing schizophrenia. However, it is not known whether C4 plays a causative role in this brain disorder. Using confocal imaging and whole-cell electrophysiology, Comer et al. demonstrate that overexpression of C4 in mouse prefrontal cortex neurons leads to perturbations in dendritic spine development and hypoconnectivity, which mirror neuropathologies found in schizophrenia patients. They also find evidence that microglia-mediated synaptic engulfment is enhanced with increased expression of C4, and that C4-dependent circuit dysfunction in the frontal cortex leads to decreased social interactions in juvenile and adult mice. The image shows a confocal fluorescent micrograph of part of the mouse prefrontal cortex. Overexpression of complement C4 was achieved by introducing a plasmid containing a C4 transgene (green; the plasmid also encoded green fluorescent protein) into layer 2/3 pyramidal neurons. Microglia are stained using an antibody against Iba1 (magenta), and nuclei are stained with DAPI (blue).

Image Credit: Thanh P. H. Nguyen

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Increased expression of schizophrenia-associated gene C4 leads to hypoconnectivity of prefrontal cortex and reduced social interaction

Ashley L. Comer, Tushare Jinadasa, Balaji Sriram, Rhushikesh A. Phadke, Lisa N. Kretsge, Thanh P. H. Nguyen, Giovanna Antognetti, James P. Gilbert, Jungjoon Lee, Elena R. Newmark, Frances S. Hausmann, SaraAnn Rosenthal, Kevin Liu Kot, Yenyu Liu, William W. Yen, Borislav Dejanovic, Alberto Cruz-Martín

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