SOD1 and amyotrophic lateral sclerosis: Using the SOD1G93A transgenic mouse model (Gly93→Ala substitution in Cu/Zn superoxide dismutase 1, SOD), which expresses a high level of human mutant SOD1 and faithfully recapitulates a vast majority of the pathological abnormalities seen in ALS patients [20], we previously found that SOD1G93A MNs are hyperexcitable prenatally at E17.5 because of shorter dendritic trees and increased input resistance [3].