To investigate the altered calcium regulation of dystrophin- deficient mdx fibres we studied gene expression and localization of TRP channels in normal and dystrophic mdx skeletal muscle. Using RT-PCR and Western Blot we found TRPC3 to be similarly expressed in hindlimb muscles and diaphragm of mdx and control mice. However, immunofluorescent staining of isolated interosseus muscle fibres with an anti-TRPC3 antibody showed a more prominent fluorescence of the cytoplasm of mdx fibres while control fibres were preferentially stained at the sarcolemma. In addition muscle fibres of both genotypes revealed a cross striation pattern in agreement with a T-tubular localization of TRPC3. Incubation of mdx fibres with the unspecific Ca2+- channel blocker Gd^3+ (50 mM) resulted in a translocation of TRPC3 channels from the cytoplasm to the sarcolemma of mdx fibres within 20 min. The translocation could also be induced by nifedipine (50 mM) and 2-aminoethyldiphenylborinate (2-APB, 50 mM), but was not observed in the presence of Ca^2+-free extracellular solution. We conclude that the increased calcium influx in mdx muscle fibres cannot be explained by increased gene expression of TRPC3. The data further suggest that regulated trafficking of TRPC3 between sarcolemmal and cytoplasmic pools could be a mechanism of functional TRPC3 regulation in skeletal muscle. (Supported by BMBF, MD-Net project R14)