Trpv1-dependent Cacna1b gene inactivation reveals cell-specific functions of CaV2.2 channels in vivo
Voltage-gated CaV2.2 channels underlie the N-type current, and they regulate calcium entry at many presynaptic nerve endings to control transmitter release. A role for CaV2.2 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 CaV2.2 channels would benefit from the availability of cell-restricted knockout mouse models and particularly in dissecting behavioral responses that depend on CaV2.2 channel activity. Here, we show the importance of CaV2.2 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 CaV2.2 channels in mediating rapidly developing heat hypersensitivity and the utility of Cre-dependent inactivation of Cacna1b to discern cell-specific CaV2.2 channel functions.