It has long been known that nicotinic acetycholine receptors (nAChRs) are present in muscle fibres not only at the end plate region but also at the myotendinous junction (MTJ). Their function at the MTJ, however, is yet unknown. Recent experiments in our laboratory lead us to suggest that nAChRs at this site might be involved in muscle repair. MTJ is subject to high mechanical stress and therefore is easily damaged. We found in pure cultures of human myogenic cells that (1) the density of nAChRs in myoblasts increases markedly just before cell fusion, (2) the fusion of human myoblasts is accelerated by the presence of a cholinergic agonist acting on nAChRs and (3) human myoblasts and myotubes spontaneously release an ACh-like compound. Based on these observations we propose that in damaged muscles the nAChRs at the MTJ and those of myogenic cells are activated by the ACh-like compound these cells release. This leads to fusion of myogenic cells with damaged muscle fibres and hence promotes repair.