The distribution of α‐bungarotoxin binding sites on mammalian skeletal muscle developing in vivo

The distribution of alpha-bungarotoxin binding sites on embryonic and neonatal rat skeletal muscle fibres was determined by autoradiography. Most of the bungarotoxin binding could be inhibited by curare. This observation, together with the spatial distribution of toxin-binding sites, indicates that the distribution of bound toxin reflects that of acetylcholine (ACh) receptors on these developing muscle cells.2. At 15 days of embryogenesis, muscle fibres showed an essentially uniform distribution of receptors. By 16 days, many fibres showed an accumulation of receptors in their mid-region. This accumulation was at the same location as histochemically demonstrated cholinesterase activity.3. At 16 days ACh receptors were distributed over the entire length of the fibres, with a gradient of increasing density as the accumulation was appoached. The density of toxin binding sites in the accumulation was greater than the general level on 15 day cells, suggesting that the high junctional density does not develop solely by the loss of extrajunctional receptors.4. The accumulations of ACh receptors became more pronounced and circumscribed with embryonic development, and after birth the extent of the localizations appeared to follow the size of the neuromuscular junction. The extrajunctional receptor density decreased with development, and by 1 week after birth was undetectable by the methods used.5. The results suggest that the high junctional receptor density found on adult, innervated skeletal muscle fibres develops after the formation of the neuromuscular junction.