Behavioral Effects of Pre- And Postnatal Exposure to Individual Polychlorinated Biphenyl Congeners in Rats

Holene, Edel; Nafstad, Inger; Skaare, Janneche Utne; Bernhoft, Aksel; Engen, Pat; Sagvolden, Terje

doi:10.1897/1552-8618(1995)14[967:beopap]2.0.co;2

Cited by 8 publications

(8 citation statements)

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“…Tests for visual discrimination learning ( age 5-18 weeks ) did not reveal any significant differences in performance between PCBexposed rats and controls. However, in a later paper, the same group of investigators reported that administration of six doses of 2 g /kg PCB 126 on gestation days 10 -20 resulted in both poorer visual discrimination and hyperactivity in exposed rats relative to controls; similar, but less marked effects were seen with 2,3 0 ,4,4 0 ,5 -pentaCB (PCB 118) ( Holene et al, 1995 ). In two more recent studies, it was reported that male pups from dams exposed to PCB 153 from days 3 to 13 after delivery were hyperactive and had impaired performance in a visual discrimination test ( Holene et al, 1998 ), but female pups showed no significant differences compared with controls ( Holene et al, 1999).…”

Section: Faroon Et Almentioning

confidence: 97%

Effects of polychlorinated biphenyls on the nervous system

2000

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The neurological effects of polychlorinated biphenyls (PCBs) have been extensively investigated in humans and in animals. The main focus in human studies has been on the effects in neonates and young children, although studies of adults have also been conducted. A great deal of concern exists that even low levels of PCBs transferred to the fetus across the placenta may induce long-lasting neurological damage. Because PCBs are lipophilic substances, there is also concem that significant amounts might be transferred to nursing infants via breast milk. Studies in humans who consumed large amounts of Great Lakes fish contaminated with environmentally persistent chemicals, including PCBs. have provided evidence that PCBs are important contributors to subtle neurobehavioral alterations observed in newborn children and that some of these alterations persist during childhood. Some consistent observations at birth have been motor immaturity and hyporeflexia and lower psychomotor scores between 6 months and 2 years old. There is preliminary evidence that highly chlorinated PCB congeners, which accumulate in certain fish, are associated with neurobehavioral alterations seen in some newbom children. Subtle neurobehavioral alterations have also been observed in children bom to mothers in the general population with the highest PCB body burdens. Because of the limitations of epidemiological studies, these effects cannot be attributed entirely to PCB exposure. In one general population study, there was strong evidence that dioxins, as well as PCBs, were contributors to the neurobehavioral effects seen in exposed children. Children born to women who accidentally consumed rice oil contaminated with relatively high amounts of PCBs and chlorinated dibenzofurans (CDFs) during pregnancy also had neurodevelopmental changes. Studies in animals support the human data. Neurobehavioral alterations have been also observed in rats and monkeys following prenatal and/or postnatal exposure to commercial Aroclor mixtures, defined experimental congener mixtures, single PCB congeners, and Great Lakes contaminated fish. In addition, monkeys exposed postnatally to PCB mixtures of congeneric composition and concentration similar to that found in human breast milk showed learning deficits long after exposure had ceased. A few other generalizations can be made from the data in animals. It appears that ortho-substituted PCB congeners are more active than coplanar PCBs in modifying cognitive processes. In addition, one effect observed in both rats and monkeys--deficits on delayed spatial alternation--has been known to be induced by exposure to ortho-substituted PCBs, defined experimental mixtures, and commercial Aroclors. Both dioxin-like and non-dioxin-like PCB congeners have been shown to induce neurobehavioral alterations in animals. Changes in levels of neurotransmitters in various brain areas have also been observed in monkeys, rats, and mice. Of all the observed changes, the most consistent has been a decrease in dopamine content in basal ganglia ...

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Section: Faroon Et Almentioning

confidence: 97%

Effects of polychlorinated biphenyls on the nervous system

2000

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“…After the FI schedule, we assessed performance on a light–dark visual discrimination, a simple test of learning. Developmental PCB exposure produced deficits on visual discrimination tasks ( Holene et al 1995 ; Lilienthal and Winneke 1991 ; Rice and Hayward 1997 ), as did a commercial PBDE mixture ( Dufault et al 2005 ).…”

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confidence: 96%

Behavioral Changes in Aging but Not Young Mice after Neonatal Exposure to the Polybrominated Flame Retardant DecaBDE

Rice

Thompson

Reeve

et al. 2009

Environ Health Perspect

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BackgroundAfter several decades of commercial use, the flame-retardant chemicals polybrominated diphenyl ethers (PBDEs) and their metabolites are pervasive environmental contaminants and are detected in the human body. Decabrominated diphenyl ether (decaBDE) is currently the only PBDE in production in the United States.ObjectivesLittle is known about the health effects of decaBDE. In the present study we examined the effects of neonatal decaBDE exposure on behavior in mice at two ages.MethodsNeonatal male and female C57BL6/J mice were exposed to a daily oral dose of 0, 6, or 20 mg/kg decaBDE from postnatal days 2 through 15. Two age groups were examined: a cohort that began training during young adulthood and an aging cohort of littermates that began training at 16 months of age. Both cohorts were tested on a series of operant procedures that included a fixed-ratio 1 schedule of reinforcement, a fixed-interval (FI) 2-min schedule, and a light–dark visual discrimination.ResultsWe observed minimal effects on the light–dark discrimination in the young cohort, with no effects on the other tasks. The performance of the aging cohort was significantly affected by decaBDE. On the FI schedule, decaBDE exposure increased the overall response rate. On the light–dark discrimination, older treated mice learned the task more slowly, made fewer errors on the first-response choice of a trial but more perseverative errors after an initial error, and had lower latencies to respond compared with controls. Effects were observed in both dose groups and sexes on various measures.ConclusionsThese findings suggest that neonatal decaBDE exposure produces effects on behavioral tasks in older but not younger animals. The behavioral mechanisms responsible for the pattern of observed effects may include increased impulsivity, although further research is required.

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“…In PCB exposed rodents, grip strength was reduced (Sauer et al, 1994), reflecting impaired corticospinal tract functioning, but cliff avoidance and negative geotaxis were not delayed (Overmann et al, 1987). Hypoactivity and hyperactivity were observed (Tilson et al, 1979;Lilienthal et al, 1990;Holene et al, 1995), as well as altered swimming behavior and complex passive/active avoidance abnormalities (Pantaleoni et al, 1988). Taken together, fetal PCB and dioxin exposure may alter certain reflexive, locomotor, and adaptive behaviors that depend on normal motor development.…”

Section: Animal Models Of Human Thyroid Hormone Disordersmentioning

confidence: 98%

“…The following references were cited for hyperthyroidism: Davenport et al, 1975;Stone and Greenough, 1975;Sjoden and Soderberg, 1976. The following references were cited for PCBs and Dioxins: Reviewed in Tilson et a]., 1979;Pantaleoni et al, 1988;Van den Berg et al, 1988;Holene et al, 1995. …”

mentioning

confidence: 99%

The Effects of Thyroid Hormone Level and Action in Developing Brain: Are These Targets for the Actions of Polychlorinated Biphenyls and Dioxins?

Sher

Adams

et al. 1998

Toxicol Ind Health

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Alterations in thyroid hormone level or responsivity to thyroid hormone have significant neurologic sequelae throughout the life cycle. During fetal and early neonatal periods, disorders of thyroid hormone may lead to the development of motor and cognitive disorders. During childhood and adult life, thyroid hormone is required for neuronal maintenance as well as normal metabolic function. Those with an underlying disorder of thyroid hormone homeostasis or mitochondrial function may be at greater risk for developing cognitive, motor, or metabolic dysfunction upon exposure to substances which alter thyroid hormone economy. Polychlorinated biphenyls (PCBs) and dioxins have been argued to interfere with thyroid hormone action and thus may affect the developing and mature brain. Animal models provide useful tools for studying the effects of thyroid hormone disorders and the effects of environmental endocrine disruptors. The congenitally hypothyroid, hyt/hyt, mouse exhibits abnormalities in both the cognitive and motor systems. In this mouse and other animal models of thyroid hormone disorders, delayed somatic and reflexive development are noted, as are permanent deficits in hearing and locomotor and adaptive motor behavior. This animal's behavioral abnormalities are predicated on anatomic abnormalities in the nervous system. In turn, these abnormalities are correlated with differences in neuronal structural proteins. In normal mice, the expression of mRNAs coding for these proteins occurs temporally with the onset of autonomous thyroid hormone production. The hyt/hyt mouse has a mutation in the thyroid stimulating hormone receptor (TSHr) gene which renders it incapable of transducing the TSH signal in the thyrocyte to produce thyroid hormone. Some behavioral and possibly some biochemical abnormalities in mice exposed to PCBs are similar to those seen in the hyt/hyt mouse. In addition to direct effects on brain development and neuronal maintenance, thyroid hormone is necessary for maintaining metabolic functioning through its influence on mitochondria. Because the brain is particularly sensitive to inadequate energy generation, disorders of thyroid hormone economy also indirectly impair brain functioning. Alterations in thyroid hormone level result in differing expression of mitochondrial genes. Mutations in these mitochondrial genes lead to well-recognized syndromes of encephalomyopathy, myopathy, and multisystem disorder. Hence, PCBs and dioxins, by possibly altering the thyroid hormone milieu, may alter the functioning of mitochondria in the generation of adenosine triphosphate (ATP). The use of animal models of thyroid hormone deficiency for behavioral, anatomic, histologic, and molecular comparison will help elucidate the mechanisms of action of these putative endocrine-disrupting compounds. The study of thyroid hormone disorders provides a template for relating thyroid hormone mediated effects on the brain to these compounds.

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Behavioral Effects of Pre- And Postnatal Exposure to Individual Polychlorinated Biphenyl Congeners in Rats

Cited by 8 publications

References 0 publications

Effects of polychlorinated biphenyls on the nervous system

Effects of polychlorinated biphenyls on the nervous system

Behavioral Changes in Aging but Not Young Mice after Neonatal Exposure to the Polybrominated Flame Retardant DecaBDE

The Effects of Thyroid Hormone Level and Action in Developing Brain: Are These Targets for the Actions of Polychlorinated Biphenyls and Dioxins?

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