Abstract
Manganese (Mn), a neurotoxin causing the human disease Manganism, a Parkinson's‐like syndrome, disrupts dopamine neurotransmission in the brain. The neurotoxic mechanism of action is not fully resolved. Reports postulate manganese toxicity is more related to post‐synaptic dopamine D2 receptors (D2DR) dysfunction, than degeneration of dopamine neurons. Gill lateral ciliated cells of Crassostrea virginica are innervated by cilio‐inhibitory dopamine nerves via the branchial nerve and have D2DR type post‐synaptic receptors. Our previous physiological work found Mn treatments block the cilio‐inhibitory effect of dopamine on gill lateral cells and our immunohistofluorescence work with FITC‐labeled 2° antibodies against anti‐D2DR showed Mn treatments reduced FITC fluorescent intensity in gill lateral cells. The results suggest that either Mn toxicity causes a loss of D2DR number or a structural disruption of receptor integrity. Currently there is no effective clinical treatment for Manganism. There are reports the drug p‐aminosalicylic acid (PAS) alleviates some of the symptoms and our physiological and immunohistofluorescence studies with C. virginica showed PAS reversed the toxic action of Mn on the animals' dopaminergic system. Recently the amino acid taurine has been shown to alleviate symptoms in a number of neurodegenerative diseases. In the present study we hypothesize taurine would reverse the neurotoxic effect of Mn on gill lateral cell D2DR in C. virginica. To test this C. virginica were treated for 3 or 5 days with Mn (500 μM) followed by 3 or 5 days with taurine (500 μM), respectively. Gills were excised and treated for immunohistofluorescence as previously done. Briefly, gills were fixed in paraformaldehyde, exposed to rabbit anti‐D2DR 1° antibodies followed by FITC‐labeled goat anti‐rabbit 2° antibodies, paraffin embedded, sectioned at 10 μm and visualized on a fluorescence microscope. Fluorescence intensity was quantified using ImageJ software from NSF. Results show fluorescence intensity in gill cells of animals treated with Mn had a statistically significant decrease in fluorescence, 66% less than non‐Mn treated controls. Animals treated with 3 days of Mn followed by 3 days of taurine had gill cells showing only an 18% reduction in fluorescence intensity compared to controls. Animals treated 5 days with Mn followed by 5 days with or without taurine gave similar results. The study indicates taurine was able to reverse the Mn induced loss of post‐synaptic D2DR fluorescence similarly to what occurred with PAS treatments. The neuroprotective mechanism of taurine needs to be further investigated. This immunohistological study suggests taurine may be a promising therapeutic agent in the treatment of Manganism in humans.Support or Funding InformationThis work was supported in part by PSC‐CUNY grant 690340047, 2R25GM06003 of the Bridge Program of NIGMS and a Carnegie Foundation award.
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