Meeting Abstract

P3.103  Thursday, Jan. 6  Are the Neurotoxic Effects of Manganese Due to Blockage of Post Synaptic Dopamine Receptors NELSON, M.*; ADAMS, T.; BEAUBRUN, D.; CARROLL, M.A.; CATAPANE, E.J.; Medgar Evers College; Medgar Evers College; Kingsborough Community College; Medgar Evers College; Medgar Evers College catapane@mec.cuny.edu

Manganese (Mn) causes Manganism by disrupting dopaminergic neurotransmission, but the mechanism is unclear. p-Aminosalicylic acid (PAS) is reported an effective treatment but its mechanism is unclear. Lateral cilia of gill of Crassostrea virginica are controlled by serotonergic-dopaminergic nerves from their ganglia. Dopamine (DA) produces cilio-inhibition, serotonin (HT) cilio-excitation. Previous work showed Mn blocks cilio-inhibition of DA and is prevented by PAS. We now studied if Mn is blocking DA post-synaptic receptor binding and if PAS prevents Mn from doing this. We observed membrane potentials of lateral ciliated cells using DIBAC, a voltage sensitive fluorescent dye, while measuring cilia beating rates. Applying HT to gill or 5 Hz electrical stimulation (ES) to the branchial nerve caused prolonged membrane depolarization and increased cilia beating rates. Applying DA or 20 Hz ES after exciting cilia repolarized the cell and decreased beating rates. Mn prevented the cilio-inhibition and repolarization. This was prevented when gills were co-treated with PAS. Adding ATP to gill increased cilia beating rates without changing membrane potential. Applying MDL, an adenylcyclase inhibitor, after Mn decreased beating rates without affecting membrane potential. The study shows a correlation between membrane potential of lateral cells and cilia beating rates. It also helps elucidate the neurotoxic mechanism of action of Mn by showing the site of action is after the post-synaptic DA receptors because MDL slowed down cilia in the presence of Mn. This information is helpful to understand causes and potential therapeutic treatments of Manganism.