Abstract
Beta-N-methylamino-L-alanine, or BMAA, is a neurotoxin produced by cyanobacteria. BMAAresulting from blue-green algae blooms may negatively affect aquatic and terrestrial life, including
humans. Previous studies of BMAA effects in fish have focused on embryonic development and
have failed to address impacts in adulthood. Results from my preliminary study suggested that
BMAA has potential negative effects on the central nervous system (CNS) and locomotion within
adult zebrafish. Specifically, I observed in BMAA-exposed fish significant increases in an
apoptosis marker in the brain and decreased swimming compared to control fish. Apoptosis
labeling most often occurred in visual-motor integration areas. Further, results from fish
subsequently allowed to recover in untreated water suggested that apoptosis was maintained even
following long term removal from BMAA. I used immunohistochemistry, electrophysiology, and
behavior analysis to understand the effects of BMAA on neurochemical, physiological, and
ultimate behavioral outcomes in adult zebrafish. BMAA-exposed zebrafish had a decreased
percent change in electrical responses to a light stimulus, along with increased levels of cell death
in the retina. Despite damage to the retina, zebrafish still behaved similarly to control fish in a
preference test. Low-exposed zebrafish experienced decreased amounts of dopamine receptors
within the brain, while high-exposed fish had an increase in receptors, possibly due to injury
compensation. High-exposed zebrafish also experienced increased levels of BDNF, which may
suggest regeneration of neural tissue. Results suggest that the visual-motor system is heavily
impacted by BMAA. This work has important implications to the relationship of
neurodegenerative conditions and environmental toxins, and possible life history stage-dependent
consequences that can impact the overall health of nonhuman animals and humans alike.
