Ecotoxicology

, Volume 17, Issue 2, pp 93–101 | Cite as

Relationships among mercury, selenium, and neurochemical parameters in common loons (Gavia immer) and bald eagles (Haliaeetus leucocephalus)

  • A. M. Scheuhammer
  • N. Basu
  • N. M. Burgess
  • J. E. Elliott
  • G. D. Campbell
  • M. Wayland
  • L. Champoux
  • J. Rodrigue
Article

Abstract

Fish-eating birds can be exposed to levels of dietary methylmercury (MeHg) known or suspected to adversely affect normal behavior and reproduction, but little is known regarding Hg’s subtle effects on the avian brain. In the current study, we explored relationships among Hg, Se, and neurochemical receptors and enzymes in two fish-eating birds—common loons (Gavia immer) and bald eagles (Haliaeetus leucocephalus). In liver, both species demonstrated a wide range of total Hg (THg) concentrations, substantial demethylation of MeHg, and a co-accumulation of Hg and Se. In liver, there were molar excesses of Se over Hg up to about 50–60 μg/g THg, above which there was an approximate 1:1 molar ratio of Hg:Se in both species. However, in brain, bald eagles displayed a greater apparent ability to demethylate MeHg than common loons. There were molar excesses of Se over Hg in brains of bald eagles across the full range of THg concentrations, whereas common loons often had extreme molar excesses of Hg in their brains, with a higher proportion of THg remaining as MeHg compared with eagles. There were significant positive correlations between brain THg and muscarinic cholinergic receptor concentrations in both species studied; whereas significant negative correlations were observed between N-methyl-D-aspartic acid (NMDA) receptor levels and brain Hg concentration. There were no significant correlations between brain Se and neurochemical receptors or enzymes (cholinesterase and monoamine oxidase) in either species. Our findings suggest that there are significant differences between common loons and bald eagles with respect to cerebral metabolism and toxicodynamics of MeHg and Se. These interspecies differences may influence relative susceptibility to MeHg toxicity; however, neurochemical responses to Hg in both species were similar.

Keywords

Mercury Methylmercury Selenium Loon Eagle Neurochemistry 

Introduction

Wild birds and mammals that feed at high trophic positions in aquatic food webs can be exposed to relatively high dietary concentrations of methylmercury (MeHg). MeHg is highly neurotoxic (Clarkson and Magos 2006), and negative effects on reproduction, hormone levels, and neurochemistry in some fish and wildlife species are probable at currently realistic levels of environmental exposure (Burgess and Meyer 2007; Evers et al. 2007; Scheuhammer et al. 2007). Nevertheless, few strategies yet exist to characterize MeHg’s subclinical toxic effects on the nervous system in wildlife species.

Neurochemical changes may represent early and reversible indicators of neurological harm because they occur prior to the onset of overt functional or structural damage (Manzo et al. 2001). Among the documented neurochemical changes characteristic of MeHg exposure are disruption of glutamate uptake by astrocytes (Brookes and Kristt 1989) and inhibition of ligand binding to synaptic muscarinic cholinergic (mACh) receptors (Castoldi et al. 1996; Basu et al. 2005a). Significant correlations between brain Hg concentrations and neurochemical receptor levels (mACh, dopamine-2, and N-methyl-D-aspartic acid [NMDA] (glutamate) receptors), and enzyme activities (monomine oxidase [MAO] and cholinesterase [ChE]) were reported in feral river otters (Londra canadensis) (Basu et al. 2005b, 2007a) and mink (Mustela vison) (Basu et al. 2005c, 2007b). Some of the findings in wild mink were later verified in captive mink fed environmentally realistic levels of dietary MeHg (Basu et al. 2006, 2007b). Although a number of avian species also accumulate Hg to potentially harmful levels, neurochemical effects have yet to be characterized in birds.

Selenium (Se) can protect against the neurotoxicity of MeHg (Ganther et al. 1972; Sumino et al. 1977; Park et al. 1996; Hienz and Hoffman 1998), and correlations between Hg and Se concentrations have been reported in livers and kidneys of several fish-eating wildlife species, including common loons (Gavia immer) (Scheuhammer et al. 1998). However, the relationship between these two elements in the avian brain is currently unknown. It is also unclear whether Se can mitigate specific neurochemical effects of Hg in wildlife.

Both common loons and bald eagles (Haliaeetus leucocephalus) are high trophic predators in aquatic ecosystems, and are often considered sentinels of ecosystem health (Bowerman et al. 2002; Golden and Rattner 2003) We undertook the present study to determine: (1) if there were significant associations between Hg and Se in liver and brain tissue of common loons and bald eagles; (2) if there were significant associations between Hg concentrations and neurochemical changes (mACh and NMDA receptor binding, MAO and ChE enzyme activity) in brain tissue from these same species; (3) if Se concentrations modulated the associations between Hg and neurochemical parameters; and (4) whether species differences were apparent in any of the preceding parameters.

Methods

Animals

Carcasses of bald eagles (n = 89), from 7 Canadian provinces but primarily from Nova Scotia and British Columbia; and common loons (n = 246) from 10 Canadian provinces, but primarily from Ontario, Alberta, and Nova Scotia, were obtained from the Specimen Bank of the National Wildlife Research Centre (NWRC), Ottawa, Canada. These carcasses represent animals found dead of various causes, collected primarily during the 1990s, and whose bodies and/or tissues were subsequently archived at NWRC. For loons, most (∼80%) were adults, of which 43% were female. For eagles, data on sex and age were generally not recorded; nevertheless, almost all birds were adults or fledged immature birds. Brain and liver tissues were stored at −40°C prior to preparation for elemental and neurochemical analyses.

Mercury and selenium

Total Hg (THg), organic Hg (MeHg), and Se were measured in an accredited laboratory for metals analyses at the National Wildlife Research Center, Environment Canada using established protocols as described previously (Scheuhammer and Bond 1991; Scheuhammer et al. 1998; Neugebauer et al. 2000; Weech et al. 2004a). All elemental residue information is reported on a dry weight basis. Analytical accuracy and precision were monitored through the use of Standard Reference Materials (SRMs), and intermittent analysis of duplicate samples. SRMs included National Research Council of Canada (NRCC) DOLT-3 (dogfish liver), DORM-2 (dogfish muscle), and TORT-2 (lobster hepatopancreas). Average accuracy was within 10% of certified values for all analyses; similarly analytical precision (% Relative Standard Deviation of replicate samples) averaged <10% for all analyses.

Neurochemical receptor binding

As brain tissue was not available from all individuals, a subset of brains was used for the neurochemical assays. Cellular membranes were prepared from brain tissues using protocols described elsewhere (Basu et al. 2005a, 2006). Binding to the mACh receptor (Na/K: 50 mM NaH2PO4, 5 mM KCl, 120 mM NaCl, pH 7.4) and NMDA receptor (Tris: 50 mM Tris, 100 μM glycine, 100 μM l-glutamic acid, pH 7.4) were performed in the buffers indicated. Briefly, 30 μg of membrane preparation was re-suspended in 100 μl buffer and added to microplate wells containing a 1.0 μM GF/B glass filter (Millipore, Boston, MA, USA). For mACh receptor binding, samples were incubated with 1 nM [3H]-QNB (42 Ci/mmol; NEN/Perkin Elmer, Boston, MA, USA) for 60 min. For NMDA receptor binding, samples were incubated with 5 nM [3H]-MK-801 (22 Ci/mmol; NEN/Perkin Elmer) for 120 min. All assays were carried out under gentle agitation at room temperature and reactions were terminated by vacuum filtration. The filters were rinsed three times with buffer and then allowed to soak for 96 h in 25 μl of OptiPhase Supermix Cocktail (Perkin Elmer). Radioactivity retained by the filter was quantified by liquid scintillation counting in a microplate detector (Wallac Microbeta, Perkin Elmer) having a counting efficiency of approximately 35%. Specific binding to both receptors was defined as the difference in radioligand bound in the presence and absence of 100 μM unlabelled atropine and MK-801 for mACh and NMDA receptors, respectively. Binding was reported as fmol of radio-isotope bound per mg of membrane protein (fmol/mg). All samples were assayed in quadruplicate for total and non-specific binding. Intra- and inter-plate variation in binding was less than 9% as determined by use of internal controls.

Neurochemical enzyme activity

The activities of ChE and MAO were measured according to published procedures (Basu et al. 2007a). Tissues were sonicated for 30 s in cold Na/K buffer including 0.5% (v/v) Triton X-100. Following a 10 min centrifugation at 15,000g (4°C), the supernatant was removed. For ChE activity, 0.5 μg of supernatant protein was mixed with 100 μM 10-acetyl-3, 7-dihydroxyphenoxazine, 200 mU horseradish peroxidase, 20 mU choline oxidase, and 100 μM acetylcholine. For MAO activity, 5 μg of protein was mixed with 100 μM 10-acetyl-3, 7-dihydroxyphenoxazine, 200 mU horseradish peroxidase, and 100 mM tyramine. Following a 30 min incubation period for both assays, the reaction end-product, resorufin (λex = 540, λem = 590), was monitored between 30 and 60 min (CytoFluor 2350, Millipore, Bedford, MA, USA). Specific activities of ChE and MAO were expressed as nmol of resorufin formed per min per unit (μg or mg) protein. Each sample was assayed in triplicate. Intra- and inter-plate variation in binding was less than 7% as determined by use of internal controls.

Results

THg, MeHg, and Se in liver

Concentrations of THg in eagle liver tissue ranged from 0.5 to 104 μg/g; and in loon liver from 0.5 to 670 μg/g. For adult loons, THg in liver was significantly related to geographic region (p < 0.05, ANOVA), and an east-to-west gradient toward progressively lower liver THg concentrations was noted (Fig. 1). Due to a smaller sample size, a similar regional trend could not be assessed for eagles. However, a comparison of adult eagles from the west (British Columbia) and east (New Brunswick/Nova Scotia) coasts indicated no significant difference in liver THg concentrations (p = 0.51, t-test). Significant positive correlations in Hg concentration between liver and brain were observed for both species, with eagles tending to show higher brain-THg per unit liver-THg than loons (Fig. 2).
Fig. 1

East to west gradient of decreasing liver Hg concentrations in adult (older than hatch year) common loons from across Canada. NB = New Brunswick; NS = Nova Scotia; PEI = Prince Edward Island; ON = Ontario; PQ = Quebec; MB = Manitoba; SK = Saskatchewan; AB = Alberta; BC = British Columbia; NWT = North West Territories. Values are means ± SE; bracketed values are sample sizes. Actual values are: 134 ± 35 (NB/NS/PEI); 80 ± 9.5 (ON/QC); 32 ± 8.5 (MB/SK); 19 ± 2.5 (AB/BC); 5.2 ± 0.8 (NWT). **For NWT, no common loon samples were available; plotted values are from adults of a combination of closely related species with similar feeding habits (red throated loon, [n = 13]; yellow billed loon, [n = 4]; and Pacific loon, [n = 4]). Mercury data for these species are used in Fig. 1 for illustrative purposes only, and are not included in other analyses or graphs

Fig. 2

Relationships between THg in liver and brain of common loons (•) (log brain-THg = 0.56 log liver-THg −0.39; r = 0.80, p < 0.01) and bald eagles (□) (log brain-THg = 0.74 log liver-THg −0.21; r = 0.67; p < 0.01)

Concentrations of Se in eagle liver tissue ranged from 2.0 to 47 μg/g; and in loon liver from 1.4 to 209 μg/g. Both species showed significant positive correlations between THg and Se in liver (Fig. 3A). Because of the high sample size for common loons, the Hg–Se relationship could be described in greatest detail for this species, as follows. There was little or no relationship between THg and Se in loon liver at concentrations of THg <10 μg/g (Se = 0.52 Hg + 7.76; r = 0.17, p > 0.05, n = 63); over this range of Hg, Se concentrations were variable but averaged about 10 μg/g, perhaps reflecting normal baseline concentrations of this essential trace element. However, at THg concentrations >10 μg/g, THg and Se were highly correlated (Se = 0.25 Hg + 12.4; r = 0.84, p < 0.01, n = 178). Although there was substantial individual variability, on average there was a molar excess of Se over Hg up to about 50–60 μg/g THg in liver (or about 20 μg/g Se), after which it appeared that an approximate 1:1 molar ratio of Hg:Se was maintained (Fig. 3B). At the very highest THg concentrations (>300 μg/g in loons), the Hg:Se molar ratio was approximately 1.5. The regression model “exponential rise to a maximum value” provided a good fit for the loon (and eagle) liver THg versus Hg:Se molar ratio data (Fig. 3B). Although there were some exceptions, MeHg in liver was generally <30 μg/g, even in birds with >100 μg/g TH; the close relationship between Hg and Se at high THg concentrations is due mainly to an association between Se and inorganic Hg. Data for Hg and Se in eagle liver samples fell within the relationship described for loons; however, there were no eagle liver Hg concentrations >104 μg/g, whereas several loons had 100–700 μg/g.
Fig. 3

Relationships between THg and Se, and THg and Hg:Se molar ratio in livers of adult common loons and bald eagles. Regression coefficients (r) are for best-fit non-linear regression results using loon data only. Eagle data fall within the relationship calculated for loons, but were not used in the regression analysis. Top: Se = 8.9 + 0.33THg − 0.0002THg2 (r = 0.84, p < 0.01); Bottom: Hg:Se molar ratio = 1.39(1−0.0031THg) (r = 0.54, p < 0.01)

THg, MeHg, and Se in brain

Concentrations of THg in brain tissue were substantially lower than in liver in both species; THg in eagle brains was 0.3–23 μg/g, and in loon brains 0.2–68 μg/g. Concentrations of Se in eagle brains ranged from 0.8 to 12 μg/g; and in loon brains from 0.4 to 15 μg/g. As in liver, there was a highly significant positive correlation between THg and Se in eagle brains; however THg and Se were not well correlated in loon brains (p > 0.01; Fig. 4). There was also a distinct species difference in the proportion of MeHg in brain, especially at higher THg concentrations. At low THg concentraions (<4 μg/g), both species had >80% of THg in brain present as MeHg; however, at THg concentrations >4 μg/g, eagles averaged only 40% MeHg, whereas loons averaged 78% MeHg. Thus, in brain, eagles demonstrated more apparent demethylation, as well as increasing Se concentrations as inorganic Hg increased, in contrast to common loons which showed comparatively little demethylation and little or no evidence of increasing Se concentrations with increasing THg accumulation. The slope of the relationship “THg versus Hg:Se molar ratio” was about 40% greater in loon brain than in eagle brain indicating that molar excesses of Hg over Se would occur with less accumulation of Hg in loons than in eagles. Furthermore, there was little evidence of a maximum Hg:Se ratio in brain tissue of loons, contrary to results for liver (Fig. 5). In eagles, the Hg:Se molar ratio never exceeded 1 in the brain, whereas in loons, the Hg:Se molar ratio was as high as 16 (Fig. 5).
Fig. 4

Relationships between THg and Se in brain tissue of common loons and bald eagles. Dashed lines reflect best-fit linear regression results. Relationship is not significant for loons (r = 0.17); for eagles, best-fit linear regression is: brain Se = 0.37 brain Hg + 1.33 (r = 0.73, p < 0.01)

Fig. 5

Relationships between THg and Hg:Se molar ratio in brain tissue of common loons and bald eagles. Dashed lines indicate best-fit linear regression results. For loons: log(brain Hg:Se molar ratio) = 0.91 log(brain THg) + 1.27 (r = 0.86, p < 0.01); for eagles: log(brain Hg:Se molar ratio) = 0.60 log(brain THg) + 0.76 (r = 0.85, p < 0.01)

Neurochemical parameters

All neurochemical correlations were assessed against log-transformed values of Hg and Se. In both loons and eagles, a significant positive correlation was calculated between [3H]-QNB bound (mACh receptor density) and THg concentrations in the brain (Fig. 6A, B). The correlation with [3H]-QNB bound was also significant for brain MeHg but not inorganic Hg in both species (Table 1). For the NMDA receptor, a negative correlation was calculated between [3H]-MK-801 bound and THg concentrations in the brains of both species (Fig. 6C, D). The amount of [3H]-MK-801 bound was also correlated with inorganic Hg but not MeHg in both species (Table 1). In general, the activities of ChE and MAO were not associated with Hg levels in either species. Further, there were no associations between concentrations of brain Se with either neurochemical receptor or enzyme studied. In bald eagles, but not in common loons, significant correlations were measured between the molar ratio of Hg:Se with [3H]-QNB and [3H]-MK-801 bound (Table 1).
Fig. 6

Relationships between total Hg and neurochemical receptors (A and B: mACh receptor levels as determined by specific [3H]-QNB binding; C and D: NMDA (glutamate) receptor levels as determined by specific [3H]-MK801 binding) in the brains of wild common loons (n = 45) and bald eagles (n = 43). See Table 1 for r and p values

Table 1

Associations among Hg, Se and neurochemical receptors (mACh, NMDA) and enzymes (ChE, MAO) in the brains of wild bald eagles (n = 43) and common loons (n = 45) as determined by Pearson’s correlations

 

Receptor binding

Enzyme activity

mACh

NMDA

ChE

MAO

Common loon

THg

r = 0.41

r = −0.40

r = 0.21

r = 0.29

p = 0.005

p = 0.006

p = 0.17

p = 0.06

MeHg

r = −0.44

r = −0.25

r = 0.28

r = 0.19

p = 0.008

p = 0.14

p = 0.11

p = 0.29

Inorganic Hg

r = 0.271

r = −0.46

r = 0.10

r = 0.21

p = 0.164

p = 0.008

p = 0.65

p = 0.280

Se

r = 0.227

r = −0.10

r = 0.01

r = −0.17

p = 0.134

p = 0.50

p = 0.97

p = 0.281

Hg:Se molar ratio

r = 0.09

r = −0.25

r = 0.03

r = 0.15

p = 0.56

p = 0.11

p = 0.86

p = 0.35

Bald eagle

THg

r0.50

r = −0.44

r = −0.20

r = 0.26

p = 0.00006

p = 0.003

p = 0.21

p = 0.10

MeHg

r0.51

r = −0.172

r = −0.36

r = 0.20

p = 0.0007

p = 0.303

p = 0.03

p = 0.22

Inorganic Hg

r = 0.16

r = −0.34

r = −0.077

r = −0.04

p = 0.35

p = 0.028

p = 0.66

p = 0.83

Se

r = 0.16

r = −0.17

r = −0.172

r = 0.05

p = 0.30

p = 0.28

p = 0.28

p = 0.75

Hg:Se molar ratio

r0.70

r = −0.47

r = −0.20

r = 0.42

p = 0.0001

p = 0.001

p = 0.22

p = 0.04

Hg and Se data were log-transformed prior to analyses. Bold values indicate the most highly significant (p < 0.01) relationships

Note: mACh receptor levels determined by specific [3H]-QNB binding; NMDA (glutamate) receptor levels determined by specific [3H]-MK801 binding

Discussion

Concentrations of Hg and/or Se in livers of common loons and bald eagles analyzed in the current study were comparable to ranges reported previously for these species (Wood et al. 1996; Pokras et al. 1998; Scheuhammer et al. 1998; Bischoff et al. 2002; Stout and Trust 2002; Weech et al. 2004b). However concentrations of Hg and Se in brain tissue of these species have not been previously reported. In livers of both eagles and loons, we observed an average molar ratio Hg:Se ≈ 1.0–1.5 once THg concentrations exceeded about 50 μg/g. Most of the THg at these higher concentrations was inorganic Hg. Similarly, some predatory marine mammals such as polar bears (Ursus maritimus) also demonstrate an approximate 1:1 molar ratio of Hg:Se in liver when Hg concentrations are elevated (Braune et al. 1991; Dietz et al. 2000). However, liver is not a major target organ of MeHg toxicity, whereas the brain is. Brain THg concentrations were as high as 23 μg/g in eagles and 68 μg/g in loons, levels known to be associated with neurotoxicity and/or reproductive impairment in various avian and mammalian species (Wobeser et al. 1976; Barr 1986; Burbacher et al. 1990; Basu et al. 2007c). It may be toxicologically important that eagles showed a superior ability to demethylate MeHg in the brain, and demonstrated a positive association between THg and Se, whereas loons showed much less demethylation and poor association between THg and Se. In brains of both eagles and loons, a molar ratio of THg:Se = 1 occurred at about 8–10 μg/g THg (∼3 μg/g wet wt.); however, above this threshold, molar excesses of Hg accumulated more rapidly in loons than in eagles. Demethylation of MeHg and subsequent sequestration of inorganic Hg with Se has frequently been suggested as a probable detoxification mechanism for animals exposed to relatively high levels of dietary MeHg (Bjorkman et al. 1995; Palmisano et al. 1995; Caurant et al. 1996). As MeHg is primarily a neurotoxicant, the relative inability of the loon brain to demethylate MeHg, and/or to increase brain Se levels as Hg levels rise, indicate that loons may be more vulnerable to MeHg toxicity than eagles. Although no studies have explicitly compared the sensitivities of eagles and loons to MeHg exposure, several studies of common loons have reported significant toxic effects at environmentally realistic Hg exposures (Barr 1986; Meyer et al. 1998; Nocera and Taylor 1998; Evers et al. 2004) whereas published studies of wild bald eagles (and also osprey) have to date reported no strong associations between Hg exposure and poor reproductive success or behavioral signs of neurotoxicity in these raptorial species (Bowerman et al. 1994; Welch 1994; DesGranges et al. 1998; Weech et al. 2006). Similar differences in Hg metabolism have been reported between piscivorous Mustelid species. Relative to river otters, mink showed an inferior apparent ability to demethylate MeHg and to increase Se in their brains with increasing Hg concentrations (Evans et al. 2000; Haines et al. 2004; Basu et al. 2005b, c). Several studies have documented Hg toxicity in mink (Basu et al. 2007c), whereas there is only limited evidence in wild river otters (Wren 1985). Observed species differences in the metabolism and toxicity of MeHg may have evolutionary origins; however, potential explanations are necessarily speculative at present and are beyond the scope of our study. Collectively, the current study comparing loons and eagles, and earlier studies comparing otter and mink, suggest that interspecies differences in cerebral MeHg and Se metabolism occur. That this may render some species more vulnerable than others to MeHg toxicity is a possibility requiring further investigation.

Growing evidence suggests that ecologically relevant exposure to MeHg can exert sub-clinical damage in wild animals by affecting neurochemical signaling pathways. A major finding of the current study was that changes in neurochemical receptor (mACh and NMDA) levels were related to Hg accumulation in two fish-eating birds. Hg-associated increases in mACh receptor levels have also been documented in wild mink trapped across Canada (Basu et al. 2005c) and subsequently verified in the laboratory with captive mink fed MeHg in their diets (Basu et al. 2006). Increased levels of mACh receptor in these studies may represent an adaptive strategy to ensure neurotransmission as Hg can directly interrupt the binding of ligands to the mACh receptor (Castoldi et al. 1996; Basu et al. 2005a). This Hg-induced blockage can disrupt functional processes downstream of mACh receptor activation, including calcium homeostasis and inositol-1,4,5-triphosphate 3 generation, and ultimately lead to cell death (Limke et al. 2004).

We observed negative correlations between NMDA receptor levels and Hg concentrations in the brains of both common loons and bald eagles. Negative associations between these two parameters were also reported in the brains of wild mink as well as captive mink that were experimentally exposed to different levels of dieatary MeHg (Basu et al. 2007b). At sub-micromolar concentrations, Hg has been shown to elevate synaptic glutamate concentrations by inhibiting its uptake into astrocytes (Brookes and Kristt 1989; Juarez et al. 2002). High levels of glutamate cause excitotoxic damage via prolonged stimulation of the NDMA receptors and the concomitant increase in intraneuronal Ca2+. As an adaptive response, down-regulation of NMDA receptors is commonplace in neurological disorders that affect glutamate homeostasis, such as anoxia and ischemia (Lipton and Rosenberg 1994). Here, we provide evidence that a similar response may exist in wild birds that accumulate high burdens of Hg.

In light of the differences between eagles and loons with respect to the degree of methylation of brain Hg and the corresponding levels of brain Se, it is perhaps surprising that Hg-related neurochemical responses were similar in both species. In both species, neurochemical changes were associated primarily with changes in THg concentrations, and were generally not related to other parameters such as brain Se or inorganic:organic Hg ratios. Clearly, additional research is required to explain the basis of interspecies differences in sensitivity to MeHg exposure; and to better elucidate the mechanisms of action of Hg on brain chemistry.

Summary

Here we describe the patterns of tissue Hg and Se accumulation in 2 major fish-eating bird species (common loons and bald eagles), indicating substantial species differences especially with regard to Hg and Se accumulation in brain. Eagles showed a highly significant co-accumulation of Se with Hg, as well as efficient demethylation of MeHg, in brain whereas loons did not. We have also built upon our previous studies on wild mink and river otters to show that Hg-related neurochemical changes also occur in wild piscivorous birds. Of particular note is that both muscarinic and glutamate receptor densities were significantly correlated with brain Hg concentrations. While Se may play a role in Hg-related neurochemical effects, the mechanistic nature of these interactions warrants further investigation, particularly with respect to potential interspecies differences.

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Copyright information

© Springer Science+Business Media, LLC 2007

Authors and Affiliations

  • A. M. Scheuhammer
    • 1
  • N. Basu
    • 1
  • N. M. Burgess
    • 2
  • J. E. Elliott
    • 3
  • G. D. Campbell
    • 4
  • M. Wayland
    • 5
  • L. Champoux
    • 6
  • J. Rodrigue
    • 6
  1. 1.National Wildlife Research CentreEnvironment CanadaOttawaCanada
  2. 2.Environment Canada, Atlantic RegionMount PearlCanada
  3. 3.Environment Canada, Pacific-Yukon RegionDeltaCanada
  4. 4.Canadian Co-operative Wildlife Health NetworkUniversity of GuelphGuelphCanada
  5. 5.Environment Canada, Prairie & Northern RegionSaskatoonCanada
  6. 6.Environment Canada, Canadian Wildlife ServiceSainte-FoyCanada

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