Meeting Abstract
Atrazine is one of the most commonly used herbicides in the United States. Previous work has shown that exposure to atrazine negatively affects crayfish chemoreception, a physiological process essential to detecting food and mate odors. Our past research has also shown that after being exposed to clean water for a 72-hour period, crayfish do not recover their chemoreception abilities short term. Current data suggests that atrazine exposed crayfish are able to recover long term, regaining chemoreception within 15 days post-atrazine exposure. Due to the fact that atrazine impairs chemosensory responses, our goal for this study was to determine the effect of atrazine on olfactory sensory neurons located in the lateral antennules of crayfish. In this experiment, two groups were utilized. One group was exposed to environmentally relevant concentrations of atrazine, which included concentrations of either 80 ppb or 300 ppb respectively, for a 15-day period. The second group served as the control and was withheld from atrazine exposure. Post treatment, lateral antennules from both groups were fixed in 4% paraformaldehyde, decalcified and subsequently cryoprotected. Medial segments were then sectioned on a cryostat. Antennule cross sections were stained with antibodies against tubulin, a protein found in neurons, and DAPI, a nuclear stain and imaged. Our data shows that atrazine exposure causes degeneration of olfactory sensory neuron bundles or clusters, leading to impairments in chemosensory abilities. Overall, this research demonstrates that environmentally-relevant atrazine exposure causes structural changes in the main olfactory organ of crayfish. Future research will allow for the examination of olfactory cell death and regeneration.
