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<p>The voltage-gated calcium channel Ca<sub>V</sub>2.2 is predominantly located in neuronal synapses, where it plays a role in pain signaling and neurotransmitter release. Furthermore, Ca<sub>V</sub>2.2 is important during early central nervous system development, as it is subsequently replaced by other calcium channels. A number of mouse lines with disrupted Ca<sub>V</sub>2.2 channels have been developed through the utilization of a gene-targeting vector. The Ca<sub>V</sub>2.2-deficient mice primarily exhibited reduced anxiety-linked behavior and response to pain stimuli. In a previous study, we observed hyperactivity and seizures in Ca<sub>V</sub>2.2-knockout mice. Given the absence of prior descriptions of these characteristics, an in-depth characterization was conducted. This characterization included longitudinal behavioral studies, as well as histological, proteomic, and metabolomic analyses. Irrespective of the frequency with which testing was conducted, a variety of behaviors were observed (e.g., hyperactivity and increased exploratory behavior) in comparison with wild-type mice. The frequency and severity of the performed tests demonstrated a positive correlation with the magnitude of the difference in molecular markers between Ca<sub>V</sub>2.2-knockout and wild-type mice. Seizures were observed but were not common. These results suggest that the Ca<sub>V</sub>2.2-knockout mouse lines are susceptible to repeated stress stimuli during experimental studies. The mice are characterized by hyperactivity, explorative behavior, and sometimes experience seizures.</p>

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In-depth characterization of the CaV2.2-knockout mouse line

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月9日

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  • Katharina Wintz,
  • Felix Schumacher,
  • Clemens Pfeiffer,
  • Maja Schäfer,
  • Ian Gering,
  • Sarah Schemmert,
  • Antje Willuweit,
  • Janine Kutzsche

摘要

The voltage-gated calcium channel CaV2.2 is predominantly located in neuronal synapses, where it plays a role in pain signaling and neurotransmitter release. Furthermore, CaV2.2 is important during early central nervous system development, as it is subsequently replaced by other calcium channels. A number of mouse lines with disrupted CaV2.2 channels have been developed through the utilization of a gene-targeting vector. The CaV2.2-deficient mice primarily exhibited reduced anxiety-linked behavior and response to pain stimuli. In a previous study, we observed hyperactivity and seizures in CaV2.2-knockout mice. Given the absence of prior descriptions of these characteristics, an in-depth characterization was conducted. This characterization included longitudinal behavioral studies, as well as histological, proteomic, and metabolomic analyses. Irrespective of the frequency with which testing was conducted, a variety of behaviors were observed (e.g., hyperactivity and increased exploratory behavior) in comparison with wild-type mice. The frequency and severity of the performed tests demonstrated a positive correlation with the magnitude of the difference in molecular markers between CaV2.2-knockout and wild-type mice. Seizures were observed but were not common. These results suggest that the CaV2.2-knockout mouse lines are susceptible to repeated stress stimuli during experimental studies. The mice are characterized by hyperactivity, explorative behavior, and sometimes experience seizures.