Effects of prenatal exposure to ethanol on neocortical development: II. Cell proliferation in the ventricular and subventricular zones of the rat

Miller, Michael W.

doi:10.1002/cne.902870305

Cited by 134 publications

(65 citation statements)

References 49 publications

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“…(9,19), in the absence of normal environmental interactions (19), and is not solely a characteristic of associational cortex (Y. Atimatsu, M. Miyamoto, I. Nihonma, K. Hirata, and Y. Uratani, unpublished data). Determination of laminar position is a phenotypic trait that has been linked to the cell cycle (20,21). Even early migrating (22) LAMP-positive grafts located in the host perirhinal cortex (E12 sensorimotor and the E12 and E14 perirhinal transplants), however, demonstrates that placement itself into the lateral hemisphere is not a limiting factor.…”

Section: Resultsmentioning

confidence: 99%

Attraction of specific thalamic input by cerebral grafts depends on the molecular identity of the implant.

Barbe

Levitt

1992

Proc. Natl. Acad. Sci. U.S.A.

102

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The cerebral cortex of mammals differentiates into functionally distinct areas that exhibit unique cytoarchitecture, connectivity, and molecular characteristics. Molecular specification of cells fated for limbic cortical areas, based on the expression of the limbic system-associated membrane protein (LAMP), occurs during an early period of brain development. The correlation between this early molecular commitment and formation of specific thalamocortical connections was tested by using a transplantation paradigm. We manipulated the phenotype of donor limbic and sensorimotor neurons by placing them in different cortical areas of host animals. Labeling of transplanted tissue with the lipophilic dye 1,1'-dioctadecyl-3,3,3'3'-tetramethylindocarbocyanine was used to assay host thamic neurons projecting to the donor tissue. We found that limbic thalamic axons successfully projected into cortical transplants (i) when LAMP was expressed by early committed limbic cortical neurons, irrespective of their host location, and (ii) when LAMP was expressed by uncommitted sensorimotor progenitor cells whose fate was altered by their new host locale. Thus, the response of cortical neurons to both intrinsic and environmental cues that Influence their molecular phenotype has an important anatomical correlate, the development of specific patterns of thalamocortical connectivity.The emergence of specific phenotypes of developing neurons contributes to the assembly of distinct areal domains in the cerebral cortex. The regulation of phenotypic expression appears to be complex, influenced by an as yet ill-defined array of intrinsic and environmental factors that operate as the cortex forms during ontogeny. Some of the controversies surrounding the issue of cortical specification in the mammalian brain relate to the different effects that environmental manipulations may have on specific phenotypes. For example, the host environment appears to define the projection patterns of layer V neurons of transplanted visual or parietal cortex (1). Afferent interactions with cortical targets modulate some features ofcellular organization, such as the barrels in somatosensory cortex (2). The ontogenetic plasticity of these phenotypes has been suggested by some to indicate an absence of early cortical specification, resulting in interchangeable regions that rely on environmental interactions for histotypic and functional differentiation (3, 4).Examination of other phenotypic traits indicates that there may be some fundamental differences between areas of developing cortex. Thalamic afferent patterning in cortex seems to occur in an ordered fashion during development (5, 6), suggesting that growing fiber systems are somehow able to recognize differences in the developing cortical mantle. Previous studies showed that the limbic system-associated membrane protein (LAMP) (7, 8) is expressed early in the formation of the cerebral cortex (9), at a time [after embryonic day (E)14] when postmitotic neurons destined for limbic cortical regions migr...

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Section: Resultsmentioning

confidence: 99%

Attraction of specific thalamic input by cerebral grafts depends on the molecular identity of the implant.

Barbe

Levitt

1992

Proc. Natl. Acad. Sci. U.S.A.

102

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“…The maturation of neural stem cells plays a crucial role in the process of neuronogenesis. An early study by Barnes and Walker (37) reported a loss of hippocampal neurons from a second-trimester equivalent alcohol exposure, and significant work from Miller's lab showed alcohol-induced changes in cortical neuronogenesis (38)(39)(40). Others have shown that rats exposure to ethanol over a 2-d window from, G. D.14-15 exhibit an immediate enlargement of the, S.V.Z, suggesting, N.S.C/NPC maturation (41), disorganized cortical architecture at the end of the neuronogenic period (42), and a persistent thinning of lamina V of the rodent cerebral cortex (43), suggesting that the effects of second-trimester ethanol exposure are persistent.…”

Section: Effects Of Alcohol During Brain Growth and Developmentmentioning

confidence: 99%

Modeling the Impact of Alcohol on Cortical Development in a Dish: Strategies from Mapping Neural Stem Cell Fate

Miranda

Santillano

Camarillo

et al. 2008

Alcohol

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SummaryDuring the second trimester period, neuroepithelial stem cells give birth to millions of new neuroblasts, which migrate away from their germinal zones to populate the developing brain and terminally differentiate into neurons. During this period, large numbers of cells are also eliminated by programmed cell death. Therefore, the second trimester constitutes an important critical period for neuronal proliferation, migration, differentiation and apoptosis. Substantial evidence indicates that teratogens like ethanol can interfere with neuronal maturation. However, there is a paucity of good model systems to study early, second trimester events. In vivo models are inherently interpretatively complex because cell proliferation, migration, differentiation, and death mechanisms occur concurrently in regions like the cerebral cortex. This temporal overlap of multiple developmental critical periods makes it difficult to evaluate the relative vulnerability of any individual critical period. Our laboratory has elected to utilize fetal rodent cerebral corticalderived neurosphere cultures as an experimental model of the second-trimester ventricular neuroepithelium. This model has enabled us to use flow cytometric approaches to identify neuroepithelial stem cell and progenitor sub-populations and to show that ethanol accelerates the maturation of neural stem cells. We have also developed a simplified mitogen-withdrawal/matrixadhesion paradigm to model the exit of neuroepithelial cells from the ventricular zone towards the subventricular zone and cortical plate, and their maturation into multipolar neurons. We can treat neurosphere cultures with ethanol to mimic exposure during the period of neuroepithelial proliferation and by using the step-wise maturation model, ask questions about the impact of prior ethanol exposure on the subsequent maturation of neurons as they migrate and undergo terminal differentiation. The combination of neurosphere culture and stepwise maturation models will enable us to dissect out the contributions of specific developmental critical periods to the overall teratology of a drug of abuse like ethanol.

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“…It is well accepted that the subventricular zone (SZ) plays an important role during the period of neocortical neurogenesis, by containing stem and progenitor cells that generate neuroblasts throughout life. Interestingly, a large proportion of the cortical neurons (from the layer II/III) are born in the SZ [Miller, 1989;Tarabykin et al, 2001;Nieto et al, 2004;Noctor et al, 2004;Zimmer et al, 2004;Englund et al, 2005;Ferrere et al, 2006;Martinez-Cerdeno et al, 2006].…”

Section: State Of Research and Mouse Modelsmentioning

confidence: 99%

<i>FOXG1</i>-Related Disorders: From Clinical Description to Molecular Genetics

Florian

Bahi‐Buisson²,

Bienvenu³

2011

Mol Syndromol

100

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Rett syndrome (RTT) is a severe neurodevelopmental disease that affects approximately 1 in 10,000 live female births and is often caused by mutations in the X-linked gene encoding methyl-CpG-binding protein 2 (MECP2). Mutations in loci other than MECP2 have also been found in individuals that have been labeled as atypical RTT. Among them, a mutation in the gene forkhead box G1 (FOXG1) has been involved in the molecular aetiology of the congenital variant of RTT. The FOXG1 gene encodes a winged-helix transcriptional repressor essential for the development of the ventral telencephalon in embryonic forebrain. Later, FOXG1 continues to be expressed in neurogenetic zones of the postnatal brain. Although RTT affects quasi-exclusively girls, FOXG1 mutations have also been identified in male patients. As far as we know, about 12 point mutations and 13 cases with FOXG1 molecular abnormalities (including translocation, duplication and large deletion on the chromosome 14q12) have been described in the literature. Affected individuals with FOXG1 mutations have shown dysmorphic features and Rett-like clinical course, including normal perinatal period, postnatal microcephaly, seizures and severe mental retardation. Interestingly, the existing animal models of FOXG1 deficiency showed similar phenotype, suggesting that animal models may be a fascinating model to understand this human disease. Here, we describe the impacts of FOXG1 mutations and their associated phenotypes in human and mouse models.

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Effects of prenatal exposure to ethanol on neocortical development: II. Cell proliferation in the ventricular and subventricular zones of the rat

Cited by 134 publications

References 49 publications

Attraction of specific thalamic input by cerebral grafts depends on the molecular identity of the implant.

Attraction of specific thalamic input by cerebral grafts depends on the molecular identity of the implant.

Modeling the Impact of Alcohol on Cortical Development in a Dish: Strategies from Mapping Neural Stem Cell Fate

<i>FOXG1</i>-Related Disorders: From Clinical Description to Molecular Genetics

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