Differential effects on neuromuscular physiology between loss-of-function mutation and paraquat-induced oxidative stress in .

Oxidative stress is thought to be a major contributor to aging processes. Here, we report differential effects on neurotransmission caused by loss-of-function mutations of () and by paraquat (PQ) feeding in . We demonstrated alterations in mutants; the larval neuromuscular junction displayed supernumerary discharges and the adult giant-fiber escape pathway showed increased latency and poor response to repetitive high-frequency stimulation. Even though the concentrations used led to motor coordination defects and lethality, PQ feeding failed to reproduce such performance deficits in these larval and adult preparations, indicating mechanistic distinctions between these genetic and pharmacological manipulations of oxidative stress.