The K+ channel TASK-3 is highly expressed in cerebellar granule neurons where it encodes the K+ current IKso. Besides the role of TASK-3 in controlling cellular excitability and shaping neuronal responses, it has recently been proposed to contribute to the development and maturation of neurons in the cerebellum. K+ dependent apoptosis and tumorigenesis have also been attributed to TASK-3 over-expression. Transcription of TASK-3 is strongly dependent on depolarization-induced Ca2+-entry. To understand the mechanisms involved in TASK-3 regulation, we have characterized a minimal promoter which specifically expresses in cellular backgrounds expressing endogenous TASK-3. Moreover, we have cloned and characterized the 5' and 3' untranslated regions of TASK-3. Both regions contribute to inhibit expression of a reporter gene. Given the direct consequence of membrane potential on TASK-3 expression, this is an important first step towards the understanding of the complex regulation of this gene. (c) 2006 Elsevier Inc. All rights reserved.