Fig. 5From: Neuromuscular junction pathology is correlated with differential motor unit vulnerability in spinal and bulbar muscular atrophyNeurofilament heavy chain (NFH) localization to the axon terminal is altered in transgenic but not knock-in mice in tibialis anterior. A, C, E, G To evaluate localization of cytoskeletal structural element NFH to the axon terminal, NMJs from tibialis anterior were stained with α-BTX, synaptophysin, and SMI31 (phospho-NFH) or α -BTX, TUJ1 (BIII-tubulin, and SMI32 (unphospho-NFH) and evaluated for colocalization with the synaptophysin or α-BTX, respectively. Consistent with the trends seen in pre- and post-synaptic NMJ measurements, transgenic mice showed significantly decreased uNFH localization to the axon terminal (B; p < 0.0001) and pNFH colocalization with terminal (F; p < 0.0001) while knock-in mice did not show changes in either of these measurements (D, H). Mann–Whitney Test was used to evaluate statistical significance. uNFH Unphosphorylated neurofilament heavy chain; pNFH Phosphorylated neurofilament heavy chain; NTg Non-transgenic; Tg Transgenic; WT Wild-type; KI Knock-inBack to article page