Abstract
1. Mouse soleus muscles were denervated and some of them were chronically stimulated. Sixteen to twenty‐one days later, the number of junctional acetylcholine receptors (AChR) and their metabolic stability were examined by measuring binding of 125I‐alpha‐bungarotoxin, their gating properties by analysis of acetylcholine‐induced current fluctuations and the ultrastructure of the end‐plate membrane by electron microscopy. 2. In agreement with other studies on inactive muscles, no effect of denervation on junctional AChR number could be resolved. However, some of the fast‐gating ‘adult’ AChR channels had been replaced by slowly gating fetal AChRs, their half‐life was lowered to 38 h and the folding of the end‐plate membrane was reduced. 3. These changes were prevented in denervated but stimulated active muscles: the junctional AChR population remained homogeneously ‘adult’, the half‐life of junctional AChRs was 13 days and folding of the end‐plate membrane remained comparable to that in control muscles. 4. The significance of these results is discussed with respect to the role of muscle activity in end‐plate development.