The acute effects of an environmental neurotoxin l-bmaa on walking behavior of drosophila melanogaster: a model to study neurodegenerative diseases

Humans who have been exposed to Beta-methylamino-L-alanine (L- BMAA) developed amyotrophic lateral sclerosis Parkinson-dementia complex, (ALS-PDC). The structure of L-BMAA is similar to glutamate, making it a glutamate agonist. Since glutamate is an excitatory neurotransmitter in both insects and vertebrates, Drosophila melanogaster is an ideal model to study the effects of L-BMAA toxicity. Previous studies on fruit flies that ingested L-BMAA showed heterogeneous walking behaviors_some flies were more affected. The research outlined in this thesis studied the acute effects of L-BMAA on the locomotory behaviors of fruit flies (Canton S.) when injected with L-BMAA. The study focused on three main goals: (1) test whether injection is a better method of delivering the toxin than ingestion because it might reduce heterogeneity, (2) quantify the acute effects of injecting L-BMAA on locomotory behavior compared with the effects of more prolonged exposure by ingestion, and (3) search for evidence of sequestration or other coping mechanisms by monitoring flies for evidence for transient effects. Comparison of the two introduction routes resulted in no difference in the observed behavioral changes. Fruit flies injected with L-BMAA did not show any observable transient effects. However, this thesis project was able to shed light on the possibility of a sequestering mechanism in fruit flies to control for L-BMAA intoxication.