There is evidence that nifedipine (Nif) – a dihydropyridine (DHP) Ca 2+-channel antagonist mostly known for its L-type-specific action – is capable of blocking low voltage-activated (LVA or T-type) Ca 2+ channels as well. However, the discrimination by Nif of either various endogenous T-channel subtypes, evident from functional studies, or cloned Ca v3.1, Ca v3.2 and Ca v3.3 T-channel α1 subunits have not been determined. Here, we investigated the effects of Nif on currents induced by Ca v3.1, Ca v3.2 and Ca v3.3 expression in Xenopus oocytes or HEK-293 cells ( I α1G, I α1H and I α1I, respectively) and two kinetically distinct, “fast” and “slow”, LVA currents in thalamic neurons ( I LVA,f and I LVA,s). At voltages of the maximums of respective currents the drug most potently blocked I α1H (IC 50 = 5 μM, max block 41%) followed by I α1G (IC 50 = 109 μM, 23%) and I α1I (IC 50 = 243 μM, 47%). The mechanism of blockade included interaction with Ca v3.1, Ca v3.2 and Ca v3.3 open and inactivated states. Nif blocked thalamic I LVA,f and I LVA,s with nearly equal potency (IC 50 = 22 μM and 28 μM, respectively), but with different maximal inhibition (81% and 51%, respectively). We conclude that Ca v3.2 is the most sensitive to Nif, and that quantitative characteristics of drug action on T-type Ca 2+ channels depend on cellular system they are expressed in. Some common features in the voltage- and state-dependence of Nif action on endogenous and recombinant currents together with previous data on T-channel α1 subunits mRNA expression patterns in the thalamus point to Ca v3.1 and Ca v3.3 as the major contributors to thalamic I LVA,f and I LVA,s, respectively.