Reversible loss of acetylcholine receptor clusters at the developing rat neuromuscular junction

Abstract

Exposure of sternomastoid muscles excised from 16-day embryonic rats to medium depleted of Ca 2+ or containing high concentrations of KCl leads to extensive loss of aggregates of acetylcholine receptors newly formed at the motor end plate region. Upon restoration of Ca 2+ or removal of excess KCl, receptor accumulations reappear in the central regions of about one-third of the muscle fibers. This susceptibility of junctional AChR aggregates lasts only a short while during development of the neuromuscular junction. By the time of birth, end plate receptor aggregates have become resistant to these treatments.