Wild-Type Drosophila melanogaster Strains Respond Differentially to Rotenone Exposure

<i>Drosophila melanogaster</i> has been established as a reliable <i>in vivo</i> model for studying human diseases. However, the varied designs of such studies and the different origins of the strains have significantly contributed to metabolic and molecular differences between strains. Parkinson's disease (PD) is a neurodegenerative disorder involving the loss of dopaminergic neurons, leading to various motor and non-motor symptoms including but not limited to bradykinesia, postural instability, cognitive decline, and gut dysbiosis. Chronic exposure to toxins such as rotenone can induce neuronal cell death. We have developed a sporadic PD model by direct feeding of rotenone-supplemented food to <i>Drosophila melanogaster</i> wild-type strains, which has previously been shown to cause neuronal cell death and used to mimic PD in <i>Drosophila.</i> Upon exposure to rotenone in two wild-type strains ( <i>Oregon-R</i> and <i>Canton-S)</i> , differences in their climbing ability and lifespan were monitored. We found that the degree of motor defects upon rotenone exposure is higher in <i>Oregon-R</i> compared to age-matched <i>Canton-S</i> flies. We also observed that the <i>Canton-S</i> flies (rotenone-fed and non-rotenone-fed) exhibited a lower survival percentage than <i>Oregon-R</i> flies. However, the climbing defects in <i>Canton-S</i> flies are not as pronounced as in <i>Oregon-R</i> flies. The mechanism(s) involved in such differential effects in different wild-type <i>Drosophila</i> strains are yet to be explored and may provide a perspective on differential symptoms of PD patients belonging to different demographics.