The pharmacological properties of the expressed murine T-type α_1G channel were characterized using the whole cell patch clamp configuration. Ba²⁺ or Ca²⁺ were used as charge carriers. Both I_Ba and I_Ca were blocked by Ni²⁺ and Cd²⁺ with IC₅₀ values of 0.47±0.04 and 1.13±0.06 mM (Ni²⁺) and 162±13 and 658±23 μM (Cd²⁺), respectively. Ni²⁺, but not Cd²⁺, modified the gating of channel activation. Ni²⁺ consistently accelerated channel deactivation while Cd²⁺ had a similar effect only on I_Ca. The α_1G channel was potently blocked by mibefradil in a dose- and voltage-dependent manner. I_Ba was moderately blocked by phenytoin (IC₅₀ 73.9±1.9 μM) and was resistant to the block by valproate. Also 3 mM ethosuximide blocked 20 and 35% of the I_Ba at a HP of −100 and −60 mV, respectively, while 5 mM amiloride inhibited I_Ba by 38% and significantly slowed current activation. The α_1G channel was not affected by 10 μM tetrodotoxin. Both 1 μM (+)isradipine and 10 μM nifedipine inhibited 18 and 14% of I_Ba amplitude at a HP of −100 mV, and 23% and 29% of I_Ba amplitude at a HP of −60 mV, respectively. The α_1G current was minimally activated by 1 μM Bay K 8644.