Neurotoxic effects of manganese on GABAergic Iinervation in the bivalve mollusc Crassostrea virginica

Abstract

High levels of airborne manganese (Mn) cause Manganism a Parkinsons‐like disease in humans by interfering with dopamine (DA) neurotransmission. Studies are showing GABA neurons also are damaged by Mn. C. virginica contains a DA and serotonin (HT) innvervation of its gill. Previously we showed Mn disrupts DA innervation. We also showed the cerebral ganglia (CG) contains GABA and within the CG GABA inhibits HT innervation of gill. Here we studied if ganglia and peripheral tissues contain GABA receptors, and if Mn effects GABA neurons within CG of C. virginica. We used 1Eantibodies (GABAA Ra1–6 ) and 2E antibodies (IgG‐FITC) to detect GABA receptors. We found GABA receptors in CG, visceral ganglia, palps and digestive tract. We also examined effects of Mn on GABA inhibition of HT neurons in CG. Beating of lateral cilia in gill cells were measured by stroboscopic microscopy. Applying HT to CG caused a dose‐dependent increase in beating. Applying GABA prior to HT prevented the increase. Acute applications of Mn (50 and 500 FM) prior to GABA prevented GABA from inhibiting HT. The study shows GABA receptors present in ganglia and peripheral tissues in C. virginica and acute Mn treatments damages GABA neurons. C. virginica preparations are good, simple test preparation to study the GABAergic system and the mechanism underlying the neurotoxic effects of Mn. The work was supported by 0516041171of NYSDOE and 0622197 of DUE Program of NSF.