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The auxiliary α 2 δ calcium channel subunits play key roles in voltage-gated calcium channel function. Independent of this, α 2 δ-1 has also been suggested to be important for synaptogenesis. Using an epitope-tagged knockin mouse strategy, we examined the effect of α 2 δ-1 on Ca V 2.2 localization in the pain pathway in vivo, where Ca V 2.2 is important for nociceptive transmission and α 2 δ-1 plays a critical role in neuropathic pain. We find Ca V 2.2 is preferentially expressed on the plasma membrane of calcitonin gene-related peptide-positive small nociceptors. This is paralleled by strong presynaptic expression of Ca V 2.2 in the superficial spinal cord dorsal horn. EM-immunogold localization shows Ca V 2.2 predominantly in active zones of glomerular primary afferent terminals. Genetic ablation of α 2 δ-1 abolishes Ca V 2.2 cell-surface expression in dorsal root ganglion neurons and dramatically reduces dorsal horn expression. There was no effect of α 2 δ-1 knockout on other dorsal horn pre- and postsynaptic markers, indicating the primary afferent pathways are not otherwise affected by α 2 δ-1 ablation.

Ablation of α 2 δ-1 inhibits cell-surface trafficking of endogenous N-type calcium channels in the pain pathway in vivo

Ablation of α ₂ δ-1 inhibits cell-surface trafficking of endogenous N-type calcium channels in the pain pathway in vivo