A-type potassium current generated by the K(V)4 family of channels is an important factor regulating the frequency, latency and dendritic backpropagation of spike discharge. The K(V)4.2 complex of K(V)4.2-KChIP3-DPP10c was recently shown to form a novel signaling complex through its association with T-type Ca(V)3.2 or Ca(V)3.3 calcium channel isoforms. Ca(V)3-mediated calcium entry was shown to selectively right-shift the inactivation voltage of K(V)4.2 into the physiological range to modulate cerebellar stellate cell latency and gain. We now show that Ca(V)3.1 calcium channels can also associate with the K(V)4.2 complex to effect similar regulation of K(V)4.2 inactivation voltage. By comparison, no calcium-dependent shift in K(V)4.2 inactivation properties was elicited by any of Ca(V)1.4, Ca(V)2.1 or Ca(V)2.3 calcium channels coexpressed with the K(V)4.2 complex, emphasizing the important role for low voltage-activated Ca(V)3 channels in this signaling complex.