Excitation-Contraction coupling Muscle mass and fiber size undergo to rapid and significant changes according to environmental and pathological conditions. Among the various trophic signals, intrinsic muscle contractile activity, neurotransmission and neurotrophic factors are crucial components regulating the integrity of muscle mass. Alterations in the pattern of nerve-evoked electrical activity convey in a modulation of the signal, due to modification in the gene expression by switching on and off specific transcription factors. This excitation-transcription (E-T) coupling is crucial for isotypic determination of muscle fibers but also for plastic adaptation and compensation after the loss of muscle mass. When electrical activity is impaired, such as during neuromuscular diseases, disuse or aging, massive muscle atrophy is observed. Few components of this compensatory response have been identified; in particular, a crucial role is played by the GDF5/Smad4 pathway. Nevertheless, it is still unknown which protein acts as first trigger of the atrophic-compensatory response after an electrical activity alteration. Good candidates could be molecules implicated in the muscle voltage sensing, and we focused our study on the beta subunit of the L-type of calcium channel complex CaV1.1. CaVb1,