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 v 3.1, Ca v 3.2 and Ca v 3.3 T-channel α1 subunits have not been determined. Here, we investigated the effects of Nif on currents induced by Ca v 3.1, Ca v 3.2 and Ca v 3.3 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 =5μM, max block 41%) followed by I α1G (IC 50 =109μM, 23%) and I α1I (IC 50 =243μM, 47%). The mechanism of blockade included interaction with Ca v 3.1, Ca v 3.2 and Ca v 3.3 open and inactivated states. Nif blocked thalamic I LVA,f and I LVA,s with nearly equal potency (IC 50 =22μM and 28μM, respectively), but with different maximal inhibition (81% and 51%, respectively). We conclude that Ca v 3.2 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 v 3.1 and Ca v 3.3 as the major contributors to thalamic I LVA,f and I LVA,s , respectively.