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Fish-eating wildlife, such as river otters (Lontra canadensis), accumulate mercury (Hg) at concentrations known to impair animal behavior, but few studies have explored the underlying biochemical changes that precede clinical neurotoxicity. The objective of this study was to determine if Hg exposure can be related to concentrations of neurochemical receptors in river otters. River otter carcasses (n = 66) were collected in Ontario and Nova Scotia (Canada) by local trappers in 2002-2004. Concentrations of Hg (total and organic) were measured in the cerebral cortex and cerebellum. Saturation binding curves for the cholinergic muscarinic acetylcholine (mACh) receptor and dopamine-2 (D2) receptor were completed for each animal to calculate receptor density (Bmax) and ligand affinity (Kd). Negative correlations were found between concentrations of Hg and mACh receptor Bmax (r(total) Hg = -0.458, r(inorganic) Hg = -0.454, r(organic) Hg = -0.443) in the cerebral cortex. A negative correlation was also found between concentrations of total Hg and D2 receptor Bmax (r = -0.292) in the cerebral cortex. These results suggest that neurochemical receptors may prove useful as novel biomarkers of Hg exposure and neurotoxic effects in wildlife. Given the importance of cholinergic and dopaminergic systems in animal physiology, the ecological implications of these changes need to be investigated.

The effects of methylmercury (MeHg) on components of the cholinergic system were evaluated in captive mink (Mustela vison). Cholinergic parameters were measured in brain regions (occipital cortex, cerebellum, brain stem, basal ganglia) and blood (whole blood, plasma, serum) following an 89-day exposure to MeHg at dietary concentrations of 0, 0.1, 0.5, 1, and 2 ppm (n = 12 animals per treatment). There were no effects of MeHg on brain choline acetyltransferase, acetylcholine, and choline transporter. However, significantly higher densities of muscarinic cholinergic receptors, as assessed by 3H-quinuclidinyl benzilate binding, were measured in the occipital cortex (30.2 and 39.0% higher in the 1 and 2 ppm groups, respectively), basal ganglia (67.5 and 69.1% higher in the 0.5 and 1 ppm groups, respectively), and brain stem (64.4% higher in the 0.5 ppm group), compared to nonexposed controls. The calculated positive relationship between MeHg exposure and muscarinic cholinergic receptor levels in this dosing study were consistent with observations in wild mink. There were no MeHg-related effects on blood cholinesterase (ChE) activity, but ChE activity was significantly higher in the occipital cortex (17.0% in the 1 ppm group) and basal ganglia (34.1% in the 0.5 ppm group), compared to nonexposed controls. The parallel increases in muscarinic cholinergic receptor levels and ChE activity following MeHg exposure highlight the autoregulatory nature of cholinergic neurotransmission. In conclusion, these laboratory data support findings from wild mink and demonstrate that ecologically relevant exposures to MeHg (i.e., 0.5 ppm in diet) have the potential to alter the cholinergic system in specific brain regions.

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