SOD1 and amyotrophic lateral sclerosis: By functional comparison of MNs from the hypoglossal (hMN) and from the oculomotor nucleus (oMN) in the most commonly utilized mouse model of ALS that express a human disease causing G93A SOD1 mutation (SOD1G93A mice), we recently identified a Ca2+ homeostasis deficit, selectively in highly vulnerable hMNs at disease endstage (Fuchs et al., 2013).