Meeting Abstract
In 1991, Imidacloprid (IMD), a specific neonicotinoid, was introduced to the United States and is now the largest selling insecticide in the world. IMD causes a nearly irreversible blockage of post-synaptic nicotinic acetylcholine (ACh) receptors in the central nervous system of insects. Studies suggest that both chronic and acute exposure to IMD can increase likelihood to multiple disorders in vertebrates. Furthermore, the inhibition of ACh receptors can have a profound effect on an organism’s immune response due to ACh’s anti-inflammatory effects on macrophages. The tremendous use of IMD in recent years may have added to its soil persistence and storage as well as water contamination. Thus, amphibians are the first group of vertebrates to be directly affected by IMD in their water. We hypothesized that higher levels of acetylcholinesterase (AChE) and lower antibody production will be found in Rana castesbeiana tadpoles exposed to environmental concentrations of IMD than in unexposed tadpoles. Over eight weeks, 140 R. castesbeiana tadpoles were divided into four groups: two exposed to 100ng/L of IMD and two unexposed. On the fifth week they were injected with either a novel antigen in an adjuvant or the adjuvant alone. After an additional three weeks all tadpoles were euthanized and blood samples taken. We found no significant difference in IgY levels between IMD exposed tadpoles and unexposed tadpoles. We also found no significant difference in AChE levels between exposed and unexposed tadpoles. However, we did find that after three weeks and a single injection R. castesbeiana isotype switched from IgM to IgY. As amphibians are often used as indicator species of overall environmental health, and because we found no effect at 100ng/L of IMD in water, IMD may not have drastic effects on vertebrates in the environment at these concentrations.
