The release of Ca 2+ from intracellular stores requires a compensatory countercurrent of K + . However, the nature of the LCC-channels, previously proposed for creating this countercurrent, remains unknown. To test the hypothesis that LCC-channels are involved in Ca 2+ release, it is required to find their specific blocking agent first. In this study, we aim to examine the effects of mecamylamine on LCC-channels to assess whether it can be considered as their effective blocker. Cells' nuclei were extracted from Purkinje neurons of 3 to 4-week-old Wistar rats. The rats' cerebellum was cut into thin slices, and roughly homogenized; then the nuclei-containing pellet was resuspended and transferred into the bath of an inverted microscope, where ion currents through the LCC-channels were recorded using a nucleus-attached configuration and voltage- clamp mode of the patch-clamp technique. It was found that mecamylamine (1 mmol/l), when applied to the intranuclear side of the LCC-channels, decreased the current amplitude at negative membrane potentials (by approximately 16-17% at -40 and -60 mV , respectively) and slightly increased it at positive ones. It also reduced the open probability (P o ) of the channels at the potential of -40 mV by 45%. Conversely, when mecamylamine was added to the perinuclear side of these channels, the current amplitude decreased at both positive and negative potentials, while no change of P o was registered. The side-dependent effect may indicate differences in the molecular structure between intranuclear and perinuclear domains of LCC- channels. Additionally, it was discovered that mecamylamine induces channel flickering when applied to either side of the membrane.