SignificanceA common feature of all domestic animals is their tame behavior and lack of fear for humans. Consistent with this, we have previously demonstrated that genes with a role in brain or neural development have been particularly targeted during rabbit domestication. Here we show, using high-resolution magnetic resonance imaging, that domestic rabbits have an altered brain architecture consistent with reduced emotional processing, including attention to behaviorally relevant stimulation, such as fear detection, learning, expression, and control, as well as compromised information processing. The results, here based on rabbits, are significant for understanding both domestication-induced reorganization of brain architecture and how adaptions in brain territories and networks supporting emotion, cognition, and behavior coincide with an altered behavioral repertoire.
The L-type voltage-gated Ca2+ channel gene CACNA1C is a risk gene for various psychiatric conditions, including schizophrenia and bipolar disorder. However, the cellular mechanism by which CACNA1C contributes to psychiatric disorders has not been elucidated. Here, we report that the embryonic deletion of Cacna1c in neurons destined for the cerebral cortex using an Emx1-Cre strategy disturbs spontaneous Ca2+ activity and causes abnormal brain development and anxiety. By combining computational modeling with electrophysiological membrane potential manipulation, we found that neural network activity was driven by intrinsic spontaneous Ca2+ activity in distinct progenitor cells expressing marginally increased levels of voltage-gated Ca2+ channels. MRI examination of the Cacna1c knockout mouse brains revealed volumetric differences in the neocortex, hippocampus, and periaqueductal gray. These results suggest that Cacna1c acts as a molecular switch and that its disruption during embryogenesis can perturb Ca2+ handling and neural development, which may increase susceptibility to psychiatric disease.
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