Δ9-Tetrahydrocannabinol (THC) and cannabidiol (CBD) are the most prevalent biologically active constituents of Cannabis sativa. THC is the prototypic cannabinoid CB1 receptor agonist and is psychoactive and analgesic. CBD is also analgesic, but it is not a CB1 receptor agonist. Low voltage-activated T-type calcium channels, encoded by the CaV3 gene family, regulate the excitability of many cells, including neurons involved in nociceptive processing. We examined the effects of THC and CBD on human Ca V3 channels stably expressed in human embryonic kidney 293 cells and T-type channels in mouse sensory neurons using whole-cell, patch clamp recordings. At moderately hyperpolarized potentials, THC and CBD inhibited peak CaV3.1 and CaV3.2 currents with IC50 values of ∼1 μM but were less potent on CaV3.3 channels. THC and CBD inhibited sensory neuron T-type channels by about 45% at 1 μM. However, in recordings made from a holding potential of -70 mV, 100 nM THC or CBD inhibited more than 50% of the peak CaV3.1 current. THC and CBD produced a significant hyperpolarizing shift in the steady state inactivation potentials for each of the CaV3 channels, which accounts for inhibition of channel currents. Additionally, THC caused a modest hyperpolarizing shift in the activation of CaV3.1 and CaV3.2. THC but not CBD slowed CaV3.1 and CaV3.2 deactivation and inactivation kinetics. Thus, THC and CBD inhibit CaV3 channels at pharmacologically relevant concentrations. However, THC, but not CBD, may also increase the amount of calcium entry following T-type channel activation by stabilizing open states of the channel.