Meeting Abstract

P1.181  Friday, Jan. 4  Acute effects of BMAA-induced neurodegeneration in Drosophila MEKDARA, PJ*; SHINKAWA, N; MEKDARA, NT; GOTO, JJ; MULLER, UK; California State University, Fresno; California State University, Fresno; California State University, Fresno; California State University, Fresno; California State University, Fresno pmekdara@csufresno.edu

Beta-methylamino-L-alanine (BMAA) is a non-essential amino acid that has been linked to amyotrophic lateral sclerosis (ALS), which is a severe human neurodegenerative disease. In humans, long exposure to BMAA causes Parkinson-like symptoms. The functional properties of BMAA in the nervous system are similar to glutamate, suggesting that BMAA is a glutamate agonist. Since glutamate is a major neurotransmitter in both insects and vertebrates, we used Drosophila melanogaster to study the effects of BMAA toxicity. In insects, glutamate functions as the excitatory neurotransmitter at the neuromuscular junctions, and is also a neuromodulator in the central pattern generator, making glutamate an important factor in controlling walking activity. The study (1) quantified the acute effects of BMAA injection on locomotory behavior, (2) compared these effects to the effects of injected glutamate to determine if BMAA has the same effects as glutamate, and (3) found evidence of a sequestering mechanism by observing transient effects of the toxin. Fruit flies injected with BMAA at the concentration of 12.5 mM, 25 mM, and 50 mM showed hyperactivity almost immediately. Flies injected with BMAA and glutamate differed in their walking and flight behaviors. Fruit flies injected with glutamate were able to recover from their initial locomotory deficits within one hour after injection while the symptoms of the BMAA treated flies continued. So the sequestering mechanism for glutamate seems to be less effective for BMAA.