Chronic low level lead exposure precociously induces rat glial development in vitro and in vivo

Cookman, Gillian R.; Hemmens, Susan E.; Keane, Gary; King, William; Regan, Ciaran M.

doi:10.1016/0304-3940(88)90178-4

Cited by 31 publications

(7 citation statements)

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“…Instead, the effects most consistently noted are those on synaptogenesis and dendritic arborization (42)(43)(44)(45)(46), in vivo physiological examinations of synaptic plasticity (47)(48)(49), and decrements in myelination (50,51). Changes in glutamate and y-aminobutyric acid synthesis and release (52,53) and the glutamate N-methyl-Daspartate (NMDA) receptor levels and binding affinities have also been reported in association with low-level lead exposure (54). Direct inhibitory actions of lead on NMDA receptors in the hippocampus have also been associated with and used to explain synaptic changes as well as cognitive impairments in lead-exposed rodents and children (54).…”

Section: Distinctive Neural Systems Havementioning

confidence: 99%

Workshop to identify critical windows of exposure for children's health: neurobehavioral work group summary.

Adams

Barone

LaMantia

et al. 2000

Environ Health Perspect

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This paper summarizes the deliberations of a work group charged with addressing specific questions relevant to risk estimation in developmental neurotoxicology. We focused on eight questions. a) Does it make sense to think about discrete windows of vulnerability in the development of the nervous system? If it does, which time periods are of greatest importance? b) Are there cascades of developmental disorders in the nervous system? For example, are there critical points that determine the course of development that can lead to differences in vulnerabilities at later times? c) Can information on critical windows suggest the most susceptible subgroups of children (i.e., age groups, socioeconomic status, geographic areas, race, etc.)? d) What are the gaps in existing data for the nervous system or end points of exposure to it? e) What are the best ways to examine exposure-response relationships and estimate exposures in vulnerable life stages? f) What other exposures that affect development at certain ages may interact with exposures of concern? g) How well do laboratory animal data predict human response? h) How can all of this information be used to improve risk assessment and public health (risk management)? In addressing these questions, we provide a brief overview of brain development from conception through adolescence and emphasize vulnerability to toxic insult throughout this period. Methodological issues focus on major variables that influence exposure or its detection through disruptions of behavior, neuroanatomy, or neurochemical end points. Supportive evidence from studies of major neurotoxicants is provided. Key words: abnormal neurological development, behavioral teratology, behavioral testing methodology, delayed neurotoxicity, developmental disorders, developmental neurotoxicology, environmental health, neurobiological substrates of function, neuronal plasticity. -Environ Health Perspect 1 08(suppl 3): 535-544 (2000). http.//ehpnetl.niehs.nih.gov/docs/2000/suppl-3/535-544adams/abstract.html

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Section: Distinctive Neural Systems Havementioning

confidence: 99%

Workshop to identify critical windows of exposure for children's health: neurobehavioral work group summary.

Adams

Barone

LaMantia

et al. 2000

Environ Health Perspect

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“…Delays in cell acquisition and positioning and fibre elabo ration could result in a retarded desialylation of embryonic NCAM, however, there is little evidence for this suggestion. Although lead lengthens the neural-cell cycle in a non specific manner, it does not appear to impair cell acquisition during the postnatal struc turing of the cerebellum [5,25], Further, lead has no effect on fibre outgrowth from spinal-cord expiants cultured on collagen matrices [26]. However, lead has been dem onstrated to have an effect on glial pheno type both in vivo and in vitro.…”

Section: Discussionmentioning

confidence: 99%

“…These exposure protocols do not compro mise pup development as whole brain/body weight, and cerebellum/whole brain ratios are indistinguishable between control and lead-exposed groups. Further, analysis of haematological parameters (white-blood cell count and haemoglobin content) indicates numerous cytoplasmic extensions which ter minate in structures resembling the glial endfeet associated with mature astrocytes [26]. In vivo chronic low-level lead preco ciously induces the developmental increase in glial-specific glutamine synthetase [26].…”

Section: Influence Of Low-level Lead On Ncam Sialylation States Durinmentioning

confidence: 99%

“…Further, analysis of haematological parameters (white-blood cell count and haemoglobin content) indicates numerous cytoplasmic extensions which ter minate in structures resembling the glial endfeet associated with mature astrocytes [26]. In vivo chronic low-level lead preco ciously induces the developmental increase in glial-specific glutamine synthetase [26]. These observations may reflect a precocious state of glial differentiation and, if cell sur face phenotype is similarly altered, the po tential to impair neuronal-cell movement along the radial processes formed by astro cytes [27], However, chronic low-level lead exposure does not impair the movement of the granule-cell perikarya on the Bergmann glia during their transit from the external to internal layer in the postnatal structuring of the cerebellum [5], Thus the lead-impaired E-to-A conversion of NCAM cannot be asso ciated with a developmental delay or gross structural alteration.…”

Section: Influence Of Low-level Lead On Ncam Sialylation States Durinmentioning

confidence: 99%

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Neuroteratological Consequences of Chronic Low-Level Lead Exposure

Regan

Keegan²

1990

Dev Pharmacol Ther

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“…This effect has been shown to be the result of decreased sialic acid production by neural cells, which produces a failure in synaptic structuring (38). For humans more brain development occurs after birth than in any other species.…”

Section: Mechanisms For Neurological Effects Of Leadmentioning

confidence: 99%

Results of Lead Research: Prenatal Exposure and Neurological Consequences

Goyer¹

1996

Environmental Health Perspectives

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JSTOR is a not-for-profit service that helps scholars, researchers, and students discover, use, and build upon a wide range of content in a trusted digital archive. We use information technology and tools to increase productivity and facilitate new forms of scholarship. For more information about JSTOR, please contact support@jstor.org.. The National Institute of Environmental Health Sciences (NIEHS) and Brogan & Partners are collaborating with JSTOR to digitize, preserve and extend access to Environmental Health Perspectives.The history of advances in the understanding of the toxic effects of lead over the past 20 years is an outstanding example of how knowledge learned from research can impact public health. Measures that have had the greatest impact on reducing exposure to lead are reduction of lead from gasoline, elimination of lead solder from canned food, removal of lead from paint, and abatement of housing containing lead-based paint. Nevertheless, continuing factors that enhance risk to lead exposure, particularly during fetal life, are low socioeconomic status, old housing with lead-containing paint, and less than ideal nutrition, particularly low dietary intake of calcium, iron, and zinc. Prenatal exposure may result from endogenous sources such as lead in the maternal skeletal system or maternal exposures from diet and the environment. Experimental studies have shown that the developing nervous system is particularly sensitive to the toxic effects of lead and that a large number of the effects in the nervous system are due to interference of lead with biochemical functions dependent on calcium ions and impairment of neuronal connections dependent on dendritic pruning. There is need for more study to determine whether these effects are a continuum of prenatal lead exposure or whether prenatal exposure to lead produces unique effects. Key words: blood lead levels, fetal brain, fetal susceptibility, lead, mechanisms of central nervous system effects, neurological effects, pregnancy, prenatal exposure, risk factors. Environ Health Perspect

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Chronic low level lead exposure precociously induces rat glial development in vitro and in vivo

Cited by 31 publications

References 10 publications

Workshop to identify critical windows of exposure for children's health: neurobehavioral work group summary.

Workshop to identify critical windows of exposure for children's health: neurobehavioral work group summary.

Neuroteratological Consequences of Chronic Low-Level Lead Exposure

Results of Lead Research: Prenatal Exposure and Neurological Consequences

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