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Significance The geneCACNA1C encodes for a calcium channel that has been linked to various psychiatric conditions, including schizophrenia and bipolar disorder, through hitherto unknown cellular mechanisms. Here, we report that deletion ofCacna1c in neurons of the developing brain disrupts spontaneous calcium activity and causes abnormal brain development and anxiety. Our results indicate that marginally alterations in the expression level ofCacna1c have major effects on the intrinsic spontaneous calcium activity of neural progenitors that play a crucial role in brain development. Thus,Cacna1c acts as a molecular switch that can increase susceptibility to psychiatric disease.

Disrupted Cacna1c gene expression perturbs spontaneous Ca 2+ activity causing abnormal brain development and increased anxiety

Disrupted Cacna1c gene expression perturbs spontaneous Ca ²⁺ activity causing abnormal brain development and increased anxiety