Abstract
Morphological changes of the neuromuscular junctions were studied ultrastructurally in the denervated and reinnervated posterior cricoarytenoid (PCA) muscle of the cat. Acetylcholinesterase (AchE) activity and acetylcholine receptors (AchR) were also investigated histochemically. The left recurrent laryngeal nerve was transected at the level of the second tracheal ring and neurorraphy was done immediately after the transection. AchE activity was demonstrated by Karnovsky and Lewis method whereas AchRs were identified by snake neurotoxin (α-bungarotoxin or erabutoxin b) which had a curare-like action. Two days after denervation nerve terminals at the neuromuscular junctions almost disapeared. Three to six weeks after denervation some primary synaptic clefts were narrowed and others were flattened while the secondary synaptic clefts were relatively preserved. The intensity of AchE activity at the neuromuscular junctions was almost same as that of the nonaffected side six weeks after denervation. Fourteen weeks after denervation AchE activity decreased. The regenerating axons appeared at the neuromuscular junctions three weeks after neurorrhaphy. An evoked electromyogram was observed at this stage. Nerve terminals were small and the secondary synaptic clefts were distorted until 22 weeks after neurorrhaphy. AchRs were detected at the neuromuscular junctions of the normal PCA muscle by snake neurotoxins. Ultrastructurally AchRs were localized at the postsynaptic membrane of the neuromuscular junctions. We were also able to demonstrate ultrastructurally calcitonin gene-related peptid (CGRP) immunoreactivity in the nerve terminals of the PCA muscle. These results strongly suggest that CGRP is involved in the regulation of the contractile function of the intrinsic laryngal muscle. The motor nerve innervation of the larynx and the neuromuscular junctions in the intrinsic laryngeal muscles
