Meeting Abstract
Manganese (Mn) causes Manganism a disease disrupting dopamine (DA) neurotransmission. The mechanism of action is not fully resolved. It’s thought Mn toxicity is more related to dysfunction of DA D2 receptors (D2DR) than degeneration of DA neurons. Gill lateral cells of Crassostrea virginica are innervated by a DA nerves from the ganglia. We showed Mn treatment blocks cilio-inhibitory effects of DA, and the post-synaptic DA receptors in gill lateral cells are D2 type. We also showed treating animals with Mn in the presence of the drug p-Aminosalicylic acid (PAS) prevented the toxic effect. We hypothesize PAS could reverse Mn toxicity when applied after Mn. We treated C. virginia 3 days with Mn (500 mM) followed by 5 days with PAS (500 mM). Gills were excised, fixed, exposed to 1º antibodies against D2DR and FITC-linked 2º antibodies, embedded and sectioned. We viewed D2DR in gill cells on a fluorescence microscope showing bright FITC fluorescence in lateral and other gill cells. Fluorescence intensity of lateral cells was quantified using ImageJ software from NSF. Intensity in sections from Mn treated animals was 40% less than controls. Animals treated with PAS after Mn exposure did not show reduced fluorescence, showing PAS reversed the Mn induced lose of post-synaptic D2DR. This study shows positive correlation between loss of D2DR fluorescence in gill lateral cells in Mn treated animals vs controls and PAS reverses toxic effects of Mn on D2DR after 3 days of Mn treatment.
