In Duchenne muscular dystrophy and its mouse model, mdx, the lack of dystrophin leads to muscle degeneration, probably due to an overload of the fibers with calcium. An increased Ca2+ influx through still unidentified ion channels seems to cause the Ca2+ overload. Thus, we studied the expression of 20 transient receptor potential (TRP) ion channels in skeletal and heart muscle tissue of mdx and C57Bl control mice. Using TaqMan RT-PCR we found that TRPC3, TRPV3 and TRPM7 were expressed in high levels in skeletal muscle, TRPC6 and TRPV4 occurred in lower levels. In mdx muscle TRPM7 and TRPV4 mRNAs were increased whereas transcripts of TRPC3, C6 and TRPV3 were reduced. Heart muscle showed a similar expression pattern of TRP channels as skeletal muscle. Using in situ hybridization and immunohistochemistry we found sarcolemmal staining of TRPC3, C6, M7 as well as TRPV4 in muscle sections of control and mdx mice. In mdx muscle a strong staining for some TRP channels was also seen in mononucleated regenerating cells. Gene expression analyses of differentiating cultured muscle showed stage specific changes of TRPV4 and TRPM4 expression. This suggests a role of TRP channels for muscle differentiation. We conclude that an altered gene expression pattern of TRP channels may contribute to the dystrophic process in mdx muscle. Supported by the BMBF (MD-NET, project R14).