Asic5, also known as bile acid-sensitive ion channel (BASIC), is an orphan member of the acid-sensing ion channels (ASICs) family, which belongs to the ENaC/DEG family. ASICs are cationic channels activated by extracellular protons, widely distributed in the nervous system and play roles in various physiological and pathological processes [2,4,5,6].

In Asic5 knockout mouse models, deletion of Asic5 impaired motor performance. This is because Asic5 deletion decreased intrinsic excitability of type II unipolar brush cells (UBCs) in the vestibulocerebellum, reducing spontaneous action potential firing. Although there was partial compensation by suppressing certain K+ currents, the overall loss of Asic5 led to altered temporal processing of vestibular input, contributing to cerebellar ataxia [1,3].

In summary, Asic5 is important for the activity of type II UBCs in the vestibulocerebellum, influencing motor coordination and balance. The Asic5 knockout mouse model has revealed its role in cerebellar ataxia, providing insights into the underlying mechanisms of movement-related disorders [1,3].