Retarded object permanence development in methylmercury exposed Macaca fascicularis infants.

Burbacher, Thomas M.; Grant, Kimberly S.; Mottet, N. Karle

doi:10.1037/0012-1649.22.6.771

Cited by 58 publications

(31 citation statements)

References 24 publications

(24 reference statements)

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“…If the infant looks longer at the novel Additionally, results of preferential-looking tests at 7 months of age and cross-modal matching tests at 1 year of age predicted children considered to be at risk for learning disabilities at 6 years of age. Development of object permanence is also retarded in infant monkeys exposed prenatally to methyl mercury (226). An assessment of concurrent predictors of IQ in children 6 years of age (227) found a high correlation between IQ and tasks that may be performed in animals, including delayed match to sample (DMTS) and conditional discrimination.…”

Section: Assessment Of Nervous System Function In Animals and Humansmentioning

confidence: 99%

Critical Periods of Vulnerability for the Developing Nervous System: Evidence from Humans and Animal Models

Rice¹,

Barone²

2000

Environmental Health Perspectives

379

183

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Section: Assessment Of Nervous System Function In Animals and Humansmentioning

confidence: 99%

Critical Periods of Vulnerability for the Developing Nervous System: Evidence from Humans and Animal Models

Rice¹,

Barone²

2000

Environmental Health Perspectives

379

183

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“…Included among these effects are impaired sensory function in nonhuman primates (Rice, 1996;Gilbert, 1982, 1990), retarded behavior in transition in rodents and nonhuman primates (Newland et al, 2004;Newland et al, 1994;Paletz et al, 2006), deficits in complex, high-rate operant behavior (Newland and Rasmussen, 2000), disrupted performance on timing in fixed-interval schedules of reinforcement (Rice, 1992), delayed object permanence (Burbacher et al, 1988;Gunderson et al, 1988b), and impaired facial recognition (Gunderson et al, 1988a). Performance on tasks that tap memory function, however, are relatively spared after developmental MeHg exposure (Elsner et al, 1988;Gilbert et al, 1993;Goldey et al, 1994;Newland and Paletz, 2000).…”

Section: Introductionmentioning

confidence: 99%

Spatial and visual discrimination reversals in adult and geriatric rats exposed during gestation to methylmercury and n−3 polyunsaturated fatty acids

et al. 2007

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Fish contain essential long chain polyunsaturated fatty acids (PUFAs), particularly docosahexaenoic acid (DHA), an omega-3 (or n-3) PUFA, but are also the main source of exposure to methylmercury (MeHg), a potent developmental neurotoxicant. Since n-3 PUFAs support neural development and function, benefits deriving from a diet rich in n-3s have been hypothesized to protect against deleterious effects of gestational MeHg exposure. To determine whether protection occurs at the behavioral level, female Long-Evans rats were exposed, in utero, to 0, 0.5, or 5 ppm of Hg as MeHg via drinking water, approximating exposures of 0, 40, and 400 μg Hg/kg/day and producing 0, 0.29, and 5.50 ppm of total Hg in the brains of siblings at birth. They also received pre-and postnatal exposure to one of two diets, both based on the AIN-93 semipurified formulation. A "fish-oil" diet was high in, and a "coconut-oil" diet was devoid of, DHA. Diets were approximately equal in α-linolenic acid and n-6 PUFAs. As adults, the rats were first assessed with a spatial discrimination reversal (SDR) procedure and later with a visual (nonspatial) discrimination reversal (VDR) procedure. MeHg increased the number of errors to criterion for both SDR and VDR during the first reversal, but effects were smaller or nonexistent on the original discrimination and on later reversals. No such MeHg-related deficits were seen when the rats were retested on SDR after two years of age. These results are consistent with previous reports and hypotheses that gestational MeHg exposure produces perseverative responding. No interactions between Diet and MeHg were found, suggesting that n-3 PUFAs do not guard against these behavioral effects. Brain Hg concentrations did not differ between the diets, either. In geriatric rats, failures to respond were less common and response latencies were shorter for rats fed the fish oil diet, suggesting that exposure to a diet rich in n-3s may lessen the impact of age-related declines in response initiation.

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“…In utero exposure to MeHg was related to delayed attainment of object permanence (61), deficits in visual recognition memory (62,63), and abnormal social behavior (64). These results, frequently based on test procedures developed for use with human infants, show that in utero exposure to MeHg is related to delays in the attainment of important cognitive milestones.…”

Section: Neurobehavioral Effects In Human Infantsmentioning

confidence: 85%

Neurobehavioral effects of developmental methylmercury exposure.

Gilbert

Grant-Webster

1995

Environ Health Perspect

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Methylmercury (MeHg) is a global environmental problem and is listed by the International Program of Chemical Safety as one of the six most dangerous chemicals in the world's environment. Human exposure to MeHg primarily occurs through the consumption of contaminated food such as fish, although catastrophic exposures due to industrial pollution have occurred. The fetus is particularly sensitive to MeHg exposure and adverse effects on infant development have been associated with levels of exposure that result in few, if any, signs of maternal clinical illness or toxicity. High levels of prenatal exposure in humans result in neurobehavioral effects such as cerebral palsy and severe mental retardation. Prenatal exposure to MeHg in communities with chronic low-level exposure is related to decreased birthweight and early sensorimotor dysfunction such as delayed onset of walking. Neurobehavioral alterations have also been documented in studies with nonhuman primates and rodents. Available information on the developmental neurotoxic effects of MeHg, particularly the neurobehavioral effects, indicates that the fetus and infant are more sensitive to adverse effects of MeHg. It is therefore recommended that pregnant women and women of childbearing age be strongly advised to limit their exposure to potential sources of MeHg. Based on results from human and animal studies on the developmental neurotoxic effects of methylmercury, the accepted reference dose should be lowered to 0.025 to 0.06 MeHg pg/kg/day. Continued research on the neurotoxic effects associated with low level developmental exposure is needed. -Environ Health Perspect 103(Suppl 6): 135-142 (1995)

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Retarded object permanence development in methylmercury exposed Macaca fascicularis infants.

Cited by 58 publications

References 24 publications

Critical Periods of Vulnerability for the Developing Nervous System: Evidence from Humans and Animal Models

Critical Periods of Vulnerability for the Developing Nervous System: Evidence from Humans and Animal Models

Spatial and visual discrimination reversals in adult and geriatric rats exposed during gestation to methylmercury and n−3 polyunsaturated fatty acids

Neurobehavioral effects of developmental methylmercury exposure.

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