Comparison of neurobehavioral changes in three inbred strains of mice prenatally exposed to methylmercury

Kim, C.-Y; Nakai, Kunihiko; Kasanuma, Yuichi; Satoh, Hiroshi

doi:10.1016/s0892-0362(99)00077-x

Cited by 44 publications

(21 citation statements)

References 19 publications

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“…Finally, the C57BL/6 strain may be relatively less sensitive to developmental MeHg exposure than other mouse strains. For example, BALB/c mice display less open-field activity following gestational MeHg exposure, whereas C57BL/6J mice were unaffected (Kim, Nakai, Kasanuma, & Satoh, 2000). Thus, the behavioral effects observed in the current study may be larger in a different mouse strain or rodent species.…”

Section: Discussionmentioning

confidence: 99%

Adolescent methylmercury exposure affects choice and delay discounting in mice

Boomhower

Newland

2016

NeuroToxicology

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The developing fetus is vulnerable to low-level exposure to methylmercury (MeHg), an environmental neurotoxicant, but the consequences of exposure during the adolescent period remain virtually unknown. The current experiments were designed to assess the effects of low-level MeHg exposure during adolescence on delay discounting, preference for small, immediate reinforcers over large, delayed ones, using a mouse model. Thirty-six male C57BL/6n mice were exposed to 0, 0.3, or 3.0 ppm mercury (as MeHg) via drinking water from postnatal day 21 through 59, encompassing the murine adolescent period. As adults, mice lever-pressed for a 0.01-cc droplet of milk solution delivered immediately or four 0.01-cc droplets delivered after a delay. Delays ranged from 1.26 to 70.79 seconds, all presented within a session. A model based on the Generalized Matching Law indicated that sensitivity to reinforcer magnitude was lower for MeHg-exposed mice relative to controls; responding in MeHg-exposed mice was relatively indifferent to the larger reinforcer. Sensitivity to reinforcer delay was reduced (delay discounting was decreased) in the 0.3-ppm group, but not in the 3.0-ppm group, compared to controls. Adolescence is a developmental period during which the brain and behavior may be vulnerable to MeHg exposure. As with gestational exposure, the effects are reflected in the impact of reinforcing stimuli.

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Section: Discussionmentioning

confidence: 99%

Adolescent methylmercury exposure affects choice and delay discounting in mice

Boomhower

Newland

2016

NeuroToxicology

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“…Developmental exposures to MeHg as well as to PS have previously been reported to alter motor activity (Emack and Matthews, 2011; Franco et al, 2006; Goulet et al, 2003; Kim et al, 2000; Montgomery et al, 2008; Patin et al, 2004), and such alterations could influence FI and/or NOR performance. Therefore, locomotor activity was measured in an automated open field arena (43.2 cm × 43.2 cm × 30.5 cm; Med Associates Inc., St. Albans, Vermont) housed in sound-attenuated enclosures ventilated by a fan for a 60 min period.…”

Section: Methodsmentioning

confidence: 99%

Sex-dependent and non-monotonic enhancement and unmasking of methylmercury neurotoxicity by prenatal stress

et al. 2014

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Methylmercury (MeHg) and prenatal stress (PS) are risk factors for neurotoxicity that may co-occur in human populations. Because they also share biological substrates and can produce common behavioral deficits, this study examined their joint effects on behavioral and neurochemical effects in male and female rats. Dams had access to 0, 0.5 or 2.5ppm MeHg chloride drinking water from two weeks prior to breeding through weaning. Half of the dams in each of these treatment groups also underwent PS on gestational days 16–17. This yielded 6 groups/gender: 0-NS, 0-PS, 0.5-NS, 0.5-PS, 2.5-NS, and 2.5-PS. Behavioral testing began in young adulthood and included Fixed Interval (FI) schedule-controlled behavior, novel object recognition (NOR) and locomotor activity, behaviors previously demonstrated to be sensitive to MeHg and/or mediated by brain mesocorticolimbic dopamine glutamate systems targeted by both MeHg and PS. Behavioral deficits were more pronounced in females and included impaired NOR recognition memory only under conditions of combined MeHg and PS, while non-monotonic reductions in FI response rates occurred, with greatest effects at the 0.5ppm concentration; the less reduced 2.5ppm FI response rates were further reduced under conditions of PS (2.5-PS). Correspondingly, many neurochemical changes produced by MeHg were only seen under conditions of PS, particularly in striatum in males and in hippocampus and nucleus accumbens in females, regions of significance to the mediation of FI and NOR performance. Collectively these findings demonstrate sex-dependent and non-monotonic effects of developmental MeHg exposure that can be unmasked or enhanced by PS, particularly for behavioral outcomes in females but for both sexes in neurochemical changes, that were observed at MeHg exposure concentrations that did not influence either reproductive outcomes or maternal behavior. Thus, assessment of risks associated with MeHg may be underestimated in the absence of other extant risk factors with which it may share common substrates and effects.

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“…Open field tests were carried out in soundproof room without any human interference, as described elsewhere (Kim et al 2000). …”

Section: Methodsmentioning

confidence: 99%

Sub-acute administration of (S)-dimethyl 2-(3-(phenyltellanyl) propanamido) succinate induces toxicity and oxidative stress in mice: unexpected effects of N-acetylcysteine

et al. 2013

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The organic tellurium compound (S)-dimethyl 2-(3-(phenyltellanyl) propanamide) succinate (TeAsp) exhibits thiol-peroxidase activity that could potentially offer protection against oxidative stress. However, data from the literature show that tellurium is a toxic agent to rodents. In order to mitigate such toxicity, N-acetylcysteine (NAC) was administered in parallel with TeAsp during 10 days. Mice were separated into four groups receiving daily injections of (A) vehicle (PBS 2.5 ml/kg, i.p. and DMSO 1 ml/kg, s.c.), (B) NAC (100 mg/kg, i.p. and DMSO s.c.), (C) PBS i.p. and TeAsp (92.5 μmol/kg, s.c), or (D) NAC plus TeAsp. TeAsp treatment started on the fourth day. Vehicle or NAC-treated animals showed an increase in body weight whereas TeAsp caused a significant reduction. Contrary to expected, NAC co-administration potentiated the toxic effect of TeAsp, causing a decrease in body weight. Vehicle, NAC or TeAsp did not affect the exploratory and motor activity in the open-field test at the end of the treatment, while the combination of NAC and TeAsp produced a significant decrease in these parameters. No DNA damage or alterations in cell viability were observed in leukocytes of treated animals. Treatments produced no or minor effects on the activities of antioxidant enzymes catalase, glutathione peroxidase and glutathione reductase, whereas the activity of the thioredoxin reductase was decreased in the brain and increased the liver of the animals in the groups receiving TeAsp or TeAsp plus NAC. In conclusion, the toxicity of TeAsp was potentiated by NAC and oxidative stress appears to play a central role in this process.Electronic supplementary materialThe online version of this article (doi:10.1186/2193-1801-2-182) contains supplementary material, which is available to authorized users.

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Comparison of neurobehavioral changes in three inbred strains of mice prenatally exposed to methylmercury

Cited by 44 publications

References 19 publications

Adolescent methylmercury exposure affects choice and delay discounting in mice

Adolescent methylmercury exposure affects choice and delay discounting in mice

Sex-dependent and non-monotonic enhancement and unmasking of methylmercury neurotoxicity by prenatal stress

Sub-acute administration of (S)-dimethyl 2-(3-(phenyltellanyl) propanamido) succinate induces toxicity and oxidative stress in mice: unexpected effects of N-acetylcysteine

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