Therefore, to address these questions we have mapped the postnatal development of functional and structural deficits at NMJs from 2 weeks of age to the onset of the first overt motor symptoms (hindlimb tremor) in vivo in the SOD1-G93A mouse model of ALS, which over-expresses the defective human SOD1 gene (hSOD1-G93A). The gene discussed is SOD1; the disease is amyotrophic lateral sclerosis.