Action　potential　induces　membrane　depolarization　and　triggers　intracellular　free　Ca2+　concentration　(Ca2+)-dependent　secretion　(CDS)　via　Ca2+　influx　through　voltage-gated　Ca2+　channels.　We　report　a　new　type　of　somatic　exocytosis　triggered　by　the　action　potential　per　se-Ca2+-independent　but　voltage-dependent　secretion　(CiVDS)-in　dorsal　root　ganglion　neurons.　Here　we　uncovered　the　molecular　mechanism　of　CiVDS,　comprising　a　voltage　sensor,　fusion　machinery,　and　their　linker.　Specifically,　the　voltage-gated　N-type　Ca2+　channel　(Ca(V)2.2)　is　the　voltage　sensor　triggering　CiVDS,　the　SNARE　complex　functions　as　the　vesicle　fusion　machinery,　the　＂synprint＇＇　of　Ca(V)2.2　serves　as　a　linker　between　the　voltage　sensor　and　the　fusion　machinery,　and　ATP　is　a　cargo　of　CiVDS　vesicles.　Thus,　CiVDS　releases　ATP　from　the　soma　while　CDS　releases　glutamate　from　presynaptic　terminals,　establishing　the　Ca(V)2.2-SNARE　＂voltage-gating　fusion　pore＇＇　as　a　novel　pathway　co-existing　with　the　canonical　＂Ca2+-gating　fusion　pore＇＇　pathway　for　neurotransmitter　release　following　action　potentials　in　primary　sensory　neurons.