Two-pore domain potassium (K_2P) channel expression is believed to underlie the developmental emergence of a potassium leak conductance [I_K(SO)] in cerebellar granule neurons (CGNs), suggesting that K_2Pfunction is an important determinant of the input conductance and resting membrane potential. To investigate the role that different K_2Pchannels may play in the regulation of CGN excitability, we generated a mouse lacking TASK-1, a K_2Pchannel known to have high expression levels in CGNs.In situhybridization and real-time PCR studies in wild-type and TASK-1 knock-outs (KOs) demonstrated that the expression of other K_2Pchannels was unaltered in CGNs. TASK-1 knock-out mice were healthy and bred normally but exhibited compromised motor performance consistent with altered cerebellar function. Whole-cell recordings from adult cerebellar slice preparations revealed that the resting excitability of mature CGNs was no different in TASK-1 KO and littermate controls. However, the modulation ofIK(SO) by extracellular Zn²⁺, ruthenium red, and H⁺was altered. TheI_K(SO)recorded from TASK-1 knock-out CGNs was no longer sensitive to alkalization and was blocked by Zn²⁺and ruthenium red. These results suggest that a TASK-1-containing channel population has been replaced by a homodimeric TASK-3 population in the TASK-1 knock-out. These data directly demonstrate that TASK-1 channels contribute to the properties ofI_K(SO)in adult CGNs. However, TASK channel subunit composition does not alter the resting excitability of CGNs but does influence sensitivity to endogenous modulators such as Zn²⁺and H⁺.