<i>Trpv1</i> -dependent <i>Cacna1b</i> gene inactivation reveals cell-specific functions of Ca <sub>V</sub> 2.2 channels <i>in vivo</i>

Voltage-gated Ca<sub>V</sub>2.2 channels underlie the N-type current, and they regulate calcium entry at many presynaptic nerve endings to control transmitter release. A role for Ca<sub>V</sub>2.2 channels has been well established in the transmission of sensory signals including noxious information using pharmacological and global gene knockout mouse models. However, investigation of the cell-specific actions of Ca<sub>V</sub>2.2 channels has been difficult due to the lack of gene-dependent knockout mouse models and particularly in dissecting behavioral responses that depend on Ca<sub>V</sub>2.2 channel activity. Here, we show the importance of Ca<sub>V</sub>2.2 channels in <i>Trpv1</i>-lineage neurons in behavioral responses to sensory stimuli using Cre-dependent inactivation of the <i>Cacna1b</i> gene. Our work shows the cell-type specificity of Ca<sub>V</sub>2.2 channels in mediating rapidly developing heat hypersensitivity and the utility of Cre-dependent inactivation of <i>Cacna1b</i> to discern cell-specific Ca<sub>V</sub>2.2 channel functions.

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Publication Details

Journal
Channels
Published
2025-12-22
DOI
https://doi.org/10.1080/19336950.2025.2594893
Citations
1
Primary Topic
Ion channel regulation and function
Type
article
Field-Weighted Citation Impact
0.81
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article

Trpv1 -dependent Cacna1b gene inactivation reveals cell-specific functions of Ca V 2.2 channels in vivo

Martín S. Sisti, Arturo Andrade, R. Meir, Diane Lipscombe
1 citations
Channels
Ion channel regulation and function
0.81
article

Trpv1 -dependent Cacna1b gene inactivation reveals cell-specific functions of Ca V 2.2 channels in vivo

Martín S. Sisti, Arturo Andrade, R. Meir, Diane Lipscombe
article en
1 citations

Abstract

Voltage-gated Ca<sub>V</sub>2.2 channels underlie the N-type current, and they regulate calcium entry at many presynaptic nerve endings to control transmitter release. A role for Ca<sub>V</sub>2.2 channels has been well established in the transmission of sensory signals including noxious information using pharmacological and global gene knockout mouse models. However, investigation of the cell-specific actions of Ca<sub>V</sub>2.2 channels has been difficult due to the lack of gene-dependent knockout mouse models and particularly in dissecting behavioral responses that depend on Ca<sub>V</sub>2.2 channel activity. Here, we show the importance of Ca<sub>V</sub>2.2 channels in <i>Trpv1</i>-lineage neurons in behavioral responses to sensory stimuli using Cre-dependent inactivation of the <i>Cacna1b</i> gene. Our work shows the cell-type specificity of Ca<sub>V</sub>2.2 channels in mediating rapidly developing heat hypersensitivity and the utility of Cre-dependent inactivation of <i>Cacna1b</i> to discern cell-specific Ca<sub>V</sub>2.2 channel functions.

ChannelsVol. 20(1)
John Brown University (US)
Openalex Percentile: Top 20%
Ion channel regulation and function
0.81
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