Trpv1 -dependent Cacna1b gene inactivation reveals cell-specific functions of Ca V 2.2 channels in vivo
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Voltage-gated Ca V 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 V 2.2 channels has been well-established in the transmission of pain information using pharmacological and global gene inactivated mouse models. However, investigation of the cell-specific actions of Ca V 2.2 channels would benefit from the availability of cell-restricted knockout mouse models and particularly in dissecting behavioral responses that depend on Ca V 2.2 channel activity. Here, we show the importance of Ca V 2.2 channels in Trpv1 -lineage neurons in behavioral responses to sensory stimuli using Cre-dependent inactivation of the Cacna1b gene. Our work shows the cell- type specificity of Ca V 2.2 channels in mediating rapidly developing heat hypersensitivity and the utility of Cre-dependent inactivation of Cacna1b to discern cell-specific Ca V 2.2 channel functions.
