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Deletion of the voltage-gated calcium channel gene, CaV1.3, reduces Purkinje cell dendritic complexity without altering cerebellar-mediated eyeblink conditioning

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By Annette J. Klomp, Martha Pace, Jacqueline B. Mehr, Cessily Hayes
| BioRxiv
Abstract Genetic variation in CACNA1D, the gene that encodes the pore-forming subunit of the L-type calcium channel CaV1.3, has been associated with increased risk for neuropsychiatric disorders that display abnormalities in cerebellar structures. We sought to clarify if deletion of CaV1.3 in mice would induce abnormalities in cerebellar cortex cytoarchitecture or synapse morphology.
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