Morphometric effects of exposure to lead during the preweaning period on the hippocampal formation of aging rats

Kawamoto, Jerrolynn C.; Vijayan, Vijaya K.; Woolley, Dorothy E.

doi:10.1016/0197-4580(84)90006-x

Cited by 5 publications

(3 citation statements)

References 25 publications

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“…Exposure during critical periods of development to a number of agents, including MAM (75), X-ray irradiation (76), ethanol (77,78), lead (79)(80)(81)(82), methyl mercury (83), triethyltin (84), inhibitors of serotonin synthesis (85), parathion (86), permethrin, diisopropyl fluorophosphate, and polychlorinated biphenyl (PCB) mixtures (87), have all been implicated in altered synaptogenesis. In general, findings from these rodent studies indicate that the effects of these agents are more restricted to synaptogenesis when they are administered postnatally during the first and second week of brain development when this process is occurring rapidly.…”

Section: Synaptogenesismentioning

confidence: 99%

Critical periods of vulnerability for the developing nervous system: evidence from humans and animal models.

Rice

Barone

2000

Environ Health Perspect

2,222

1,706

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Vulnerable periods during the development of the nervous system are sensitive to environmental insults because they are dependent on the temporal and regional emergence of critical developmental processes (i.e., proliferation, migration, differentiation, synaptogenesis, myelination, and apoptosis). Evidence from numerous sources demonstrates that neural development extends from the embryonic period through adolescence. In general, the sequence of events is comparable among species, although the time scales are considerably different. Developmental exposure of animals or humans to numerous agents (e.g., X-ray irradiation, methylazoxymethanol, ethanol, lead, methyl mercury, or chlorpyrifos) demonstrates that interference with one or more of these developmental processes can lead to developmental neurotoxicity. Different behavioral domains (e.g., sensory, motor, and various cognitive functions) are subserved by different brain areas. Although there are important differences between the rodent and human brain, analogous structures can be identified. Moreover, the ontogeny of specific behaviors can be used to draw inferences regarding the maturation of specific brain structures or neural circuits in rodents and primates, including humans. Furthermore, various clinical disorders in humans (e.g., schizophrenia, dyslexia, epilepsy, and autism) may also be the result of interference with normal ontogeny of developmental processes in the nervous system. Of critical concern is the possibility that developmental exposure to neurotoxicants may result in an acceleration of age-related decline in function. This concern is compounded by the fact that developmental neurotoxicity that results in small effects can have a profound societal impact when amortized across the entire population and across the life span of humans.ImagesFigure 2Figure 3Figure 4Figure 5Figure 6Figure 8Figure 9Figure 12Figure 14Figure 16Figure 17

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Section: Synaptogenesismentioning

confidence: 99%

Critical periods of vulnerability for the developing nervous system: evidence from humans and animal models.

Rice

Barone

2000

Environ Health Perspect

2,222

1,706

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“…Effects on gross brain structure have not been evident in studies directed at understanding underlying neuropathology associated with low-level lead exposure. 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).…”

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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“…In the microarray study by Schneider et al (2011) 175 genes were identified that were differentially regulated in response to Pb 2+ -exposure in a sex-dependent manner with altered expression patterns, which may have resulted from Pb 2+ -alterations in CCAT regulation. Interestingly, the NMDA R2A mRNA in the developing rat hippocampus (Nihei & Guilarte, 1999), and mRNA NR1 splice variants were reported to alter hippocampal expression in all cornu ammonis (CA) regions when compared with controls, in response to gestation and developmental Pb 2+ -exposures; thus, evidencing altered synaptogenesis (Averill & Needleman, 1980; Kawamoto, Overmann, Woolley, & Vijayan, 1984; McCauley et al, 1982) and negatively effecting rodent learning (Guilarte & McGlothan, 2003; Guilarte, McGlothan, & Nihei, 2000). It is important to note, that none of these prior reports at that time on synaptogenesis evaluated any alterations in immature excitatory-dependent GABAergic genes in response to Pb 2+ -exposure, but rather glutamatergic events that later followed the development of the GABA-shift.…”

Section: Pb2+-alters Immediate-early Gene Induction Via the L-type Vsccmentioning

confidence: 99%

Developmental Pb2+-exposure alters KCC₂ and VSCC-β3 subunit expression patterns in the postnatal rat brain and cerebellar granule cell cultures: Implications for disrupted GABA-shifts resulting from neurotoxicant exposures.

Neuwirth¹,

Idrissi²

2021

Psychology & Neuroscience

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The neurotoxicant lead (Pb2+) has been studied extensively regarding neurodevelopmental impacts altering the glutamatergic system that persists across the life span. Recently, research has been redirected toward revisiting Pb2+-impacts on the neurodevelopment of the GABAergic system because it precedes the functional expression and activation of the glutamatergic system. Because the potassium chloride cotransporter (KCC2) drives the developmental regulatory shift from GABA-excitation-to-inhibition, and that the GABAA receptors activation can alter gene expression via excitation-dependent coupling of voltage sensitive calcium channels (VSCC), it is important to investigate how Pb2+-exposure might also alter the development, function, and activation of the GABAergic system. Here the relationship between control and 1,000 ppm perinatal Pb2+-exposed rats (i.e., from gestation to postnatal day [PND-22]) on the KCC2 spatiotemporal expression in the ventro-medial prefrontal cortex (vmPFC) and hippocampus (i.e., DG and CA-3) at PND 2, 7, 14, and 22 was examined. Additionally, the KCC2, the VSCC-β3 subunit of the L-type calcium channel and the GABA-AR-β3 subunit expression were examined in primary neuronal cerebellar granule cell cultures (CGC) 3-DIV to assess the impacts of Pb2+-exposure on the VSCC-β3 excitation-dependent coupling in altering the GABA-shift. The results showed that developmental Pb2+-exposure elevated the KCC2 expression in vmPFC at PND 2 and reduced at PND 14 and 22; whereas in the DG, the KCC2 expression was elevated at PND 2 and 7, and reduced at PND 14. In the CA-3, the KCC2 expression was elevated at PND 2 and 7. In the PNC, Pb2+ did not affect cell viability or confluence, but it reduced the expression of KCC2 irrespective of Pb2+-dosage and dose-dependently for VSCC-β3. Notably, in the CGCs the GABA-AR-β3 expression showed a curvilinear relationship with the most impacts at low- (0.05–0.1 μmol/L) and high-Pb2+ doses (1.5 μmol/L) in-vitro. The data suggest that lower levels of Pb2+-exposure, at the cellular level, reduced VSCC-β3 and KCC2 expression, thereby delaying the GABA-shift. As a result, the altered GABA-AR-β3 expression, dependent upon its ability to compensate during development, can cause differential patterns of mature KCC2 expression across brain regions at PND 22. Thus, developmental Pb2+-exposure can alter the development of the GABAergic system prior to the functional expression and activation of the glutamatergic system.

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Morphometric effects of exposure to lead during the preweaning period on the hippocampal formation of aging rats

Cited by 5 publications

References 25 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.

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

Developmental Pb2+-exposure alters KCC₂ and VSCC-β3 subunit expression patterns in the postnatal rat brain and cerebellar granule cell cultures: Implications for disrupted GABA-shifts resulting from neurotoxicant exposures.

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