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<p>Genetic variation in <i>CACNA1D</i>, the gene that encodes the pore-forming subunit of the L-type calcium channel Ca<sub>V</sub>1.3, has been associated with increased risk for neuropsychiatric disorders that display abnormalities in cerebellar structures. We sought to clarify if deletion of Ca<sub>V</sub>1.3 in mice would induce abnormalities in cerebellar cortex cytoarchitecture or synapse morphology. Since Ca<sub>V</sub>1.3 is highly expressed in cerebellar molecular layer interneurons (MLIs) and L-type channels appear to regulate GABA release from MLIs, we hypothesized that loss of Ca<sub>V</sub>1.3 would alter GABAergic synapses between MLIs and Purkinje cells (PCs) without altering MLI density or PC structure. As expected, we did not observe changes in the density of MLIs or PCs. Surprisingly, Ca<sub>V</sub>1.3 KO mice do have decreased complexity of PC dendritic arbors without differences in the number or structure of GABAergic synapses onto PCs. Loss of Ca<sub>V</sub>1.3 was not associated with impaired acquisition of delay eyeblink conditioning. Therefore, our data suggest that Ca<sub>V</sub>1.3 expression is important for PC structure but does not affect other measures of cerebellar cortex morphology or cerebellar function as assessed by delay eyeblink conditioning.</p>

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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

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年10月11日

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  • Annette Klomp,
  • Martha Pace,
  • Jacqueline Mehr,
  • Maria Fernanda Hermosillo Arrieta,
  • Cessily Hayes,
  • Anthony Fleck,
  • Shane Heiney,
  • Aislinn Williams

摘要

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. Since CaV1.3 is highly expressed in cerebellar molecular layer interneurons (MLIs) and L-type channels appear to regulate GABA release from MLIs, we hypothesized that loss of CaV1.3 would alter GABAergic synapses between MLIs and Purkinje cells (PCs) without altering MLI density or PC structure. As expected, we did not observe changes in the density of MLIs or PCs. Surprisingly, CaV1.3 KO mice do have decreased complexity of PC dendritic arbors without differences in the number or structure of GABAergic synapses onto PCs. Loss of CaV1.3 was not associated with impaired acquisition of delay eyeblink conditioning. Therefore, our data suggest that CaV1.3 expression is important for PC structure but does not affect other measures of cerebellar cortex morphology or cerebellar function as assessed by delay eyeblink conditioning.