Altered neuromuscular junction size and composition in aging rat laryngeal muscles

Age‐induced laryngeal dysfunction compromises voice, swallowing and airway protection. How aging alters the laryngeal muscles is unknown. Clearly, the fast and constant laryngeal muscle activity relies on robust life‐long communication with their motor neurons at the neuromuscular junction (NMJ). This study tested the hypothesis that aging disrupts NMJ organization in two laryngeal muscles: thyroarytenoid (TA) and posterior cricoarytenoid (PCA). We measured NMJ density and size, and mRNAs for acetylcholine receptor (AChR) subunits in TA and PCA muscles from Fischer 344xBrown Norway rats (6 and 30 mo of age). NMJ density and size were examined with FITC‐labeled α‐bungarotoxin and fluorescence microscopy. AChR subunit expression was determined by real‐time RT‐PCR. The motor innervation points of TA and PCA muscles from 30‐mo rats demonstrated decreased NMJ size, abundance and clustering. While age‐induced changes in the mRNAs coding for most AChR subunits were inconsistent, AChR γ mRNA content increased with age in both PCA and TA. This finding typically correlates with loss of junctional folds and is characteristic of myasthenia gravis and aging skeletal muscles. These results support our initial hypothesis and demonstrate that NMJs become smaller and less abundant in aging TA and PCA muscles. It is still unclear whether NMJ disruption is due to a corresponding loss of motor neurons. Supported by NIDCD