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p‐Aminosalicylic acid prevents the loss of immunofluorescence emissions of postsynaptic dopamine D2 receptors due to manganese treatment (796.1)
Author(s) -
Chekayev Yelena,
LoneyWalsh Kurt,
Carroll Margaret,
Catapane Edward
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.796.1
Subject(s) - receptor , dopamine receptor d2 , chemistry , dopamine receptor , dopamine , medicine , biophysics , endocrinology , biology , biochemistry
Manganese (Mn) a neurotoxin causing Manganism, a Parkinsons‐like disease, disrupts dopamine (DA) neurons. The neurotoxic mechanism is not fully resolved. It’s postulated more related to dysfunction of DA D2 receptors than degeneration of DA neurons. Crassostrea virginica gill lateral cells are innervated by DA nerves and have D2 post‐synaptic receptors. Mn blocks cilio‐inhibition of DA. PAS (p‐aminosalicylic acid) blocks the effects of Mn. It’s questioned if Mn decreases the number of DA D2 receptors in brain. We used 1̊ antibodies against D2 receptors and FITC‐linked 2̊ antibodies to quantify DA D2 receptors to test if Mn decreases the number of receptors in gill of C. virginica and if PAS prevents the decrease. We treated animals with 500 µM of Mn for up to 6 days. Sections were viewed on a fluorescence microscope, intensity was quantified with ImageJ software. Control gills had bright fluorescence corresponding to lateral and other gill cells. Intensity from animals treated up to 6 days with Mn showed a decrease up to 36% of controls. Animals co‐treated with Mn and PAS did not show reduced fluorescence. The study shows negative correlation between fluorescence intensity of DA D2 receptors in Mn treated animals vs controls and PAS negates effects of Mn. Whether intensity loss is due to decrease in D2 receptor number or altering of protein conformation and ligand binding site of D2 receptors needs to be further explored. Grant Funding Source : NIH‐ 2R25GM06003, NSF‐ 0622197, NYSED‐ 0516041071