Besides the nerve endings, the soma of trigeminal neurons also respond to membrane depolarizations with the release of neurotransmitters and neuromodulators in the extracellular space within the ganglion, a process potentially important for the cross‐communication between neighboring sensory neurons. In this study, we addressed the dependence of somatic release on Ca2+ influx in trigeminal neurons and the involvement of the different types of voltage‐gated Ca2+ (Cav) channels in the process. Similar to the closely related dorsal root ganglion neurons, we found two kinetically distinct components of somatic release, a faster component stimulated by voltage but independent of the Ca2+ influx, and a slower component triggered by Ca2+ influx. The Ca2+‐dependent component was inhibited 80% by ω‐conotoxin‐MVIIC, an inhibitor of both N‐ and P/Q‐type Cav channels, and 55% by the P/Q‐type selective inhibitor ω‐agatoxin‐IVA. The selective L‐type Ca2+ channel inhibitor nimodipine was instead without effect. These results suggest a major involvement of N‐ and P/Q‐, but not L‐type Cav channels in the somatic release of trigeminal neurons. Thus antinociceptive Cav channel antagonists acting on the N‐ and P/Q‐type channels may exert their function by also modulating the somatic release and cross‐communication between sensory neurons.