Embryonic brain enlargement requires cerebrospinal fluid pressure

Desmond, Mary E.; Jacobson, Antone G.

doi:10.1016/0012-1606(77)90364-5

Cited by 233 publications

(221 citation statements)

References 21 publications

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“…For external factors, the cerebrospinal fluid pressure inside the neural tube cavity has been demonstrated to be an essential force of brain enlargement (12). Furthermore, it has been proposed that a radially anisotropic architecture of the NE is necessary to convert the internally generated hydrostatic pressure into surface tension for tangential expansion (11).…”

Section: Discussionmentioning

confidence: 99%

“…Another intriguing possibility is that the apical-basal polarity of NE may contribute to the balloon-like enlargement of the telencephalic vesicle, because the polarized distribution of adherens junctions and the associated cytoskeletal proteins along with the vertical nestin-positive fibers produce a radially anisotropic (nonrandom) architecture of the telencephalic NE. It has been suggested that a radially anisotropic neuroepithelial wall, working against internally generated hydrostatic pressure, generates surface tension leading to tangential expansion of the telencephalic vesicle (11,12). A rapid expansion of the telencephalic vesicle may be a prerequisite for its separation into two cerebral hemispheres.…”

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confidence: 99%

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Cdc42 deficiency causes Sonic hedgehog-independent holoprosencephaly

Chen

Liao

Yang

et al. 2006

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

116

115

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The telencephalic neuroepithelium (NE) of mammalian brain has an apical-basal polarity that is marked by the positioning of neural progenitors and adherens junctions on the apical͞ventricular surface and the ascending of radial glia͞progenitor fibers toward the pial͞basal surface. The signaling pathway that establishes this apical-basal polarity of NE is not completely understood, but the Rho-family GTPase Cdc42 may play a critical role because it controls cadherin-based intercellular junctions and cell polarity in many species. Here, we tested this hypothesis by a conditional genetargeting strategy by using the Foxg1-Cre line to delete Cdc42 in the telencephalic neural progenitors in mouse embryos. We found that Cdc42-deletion abolishes the apical localization of PAR6, aPKC, E-cadherin, ␤-catenin, and Numb proteins in the NE, and severely impairs the extension of nestin-positive radial fibers. Consequently, neural progenitors were scattered throughout the entire depth of the NE, and the Cdc42-deficient telencephalon failed to bulge or separate into two cerebral hemispheres, resulting in holoprosencephaly. However, neither the midline expression of Sonic hedgehog nor the dorso-ventral patterning of the telencephalon was affected by Cdc42-deletion. Taken together, these results indicate that Cdc42 has an essential role in establishing the apicalbasal polarity of the telencephalic NE, which is needed for the expansion and bifurcation of cerebral hemispheres.neurogenesis ͉ polarity ͉ radial glia

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Cdc42 deficiency causes Sonic hedgehog-independent holoprosencephaly

Chen

Liao

Yang

et al. 2006

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

116

115

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“…Experimental data demonstrate that the loss or modification of the composition of the E-CSF strongly decreases the neuronal cell population (Desmond and Jacobson, 1977;Desmond, 1985). Moreover, Mashayesky et al (2002) and OwenLynch et al (2003) have reported that the phenotype of the mutant hydrocephalic Texas rats is due to an alteration of the proliferation of brain primordium stem cells and cortical neurogenesis due to changes in the composition of the CSF.…”

Section: E-csf Helps Control Cellular Behavior In Neuroepithelial Cellsmentioning

confidence: 99%

“…Classically, E-CSF has been involved in some epigenetic processes during early brain development, e.g., the positive pressure that drives expansion and morphogenesis Pexieder, 1968, 1970;Desmond and Jacobson, 1977), which is regulated by apical secretion of osmotically active molecules belonging to the family of proteoglycans (Gato et al, 1993;Alonso et al, 1998Alonso et al, , 1999.…”

Section: E-csf Helps Control Cellular Behavior In Neuroepithelial Cellsmentioning

confidence: 99%

“…Moreover, the fact that the protein fraction of the CSF is more complex in embryos than in adults, and that it is detected at higher concentrations, has led some authors to suggest that the E-CSF is involved in the regulation of neuroepithelial cell behavior (Dziegielewska et al, 1980b(Dziegielewska et al, , 2000Ojeda and Piedra, 2000;Miyan et al, 2003;Gato et al, 2004). In addition, it has been shown that E-CSF plays a key role in the expansion of the embryonic brain primordium at the earliest stages of development (Desmond and Jacobson, 1977;Desmond, 1985;Gato et al, 1993;Alonso et al, 1998Alonso et al, , 1999Desmond and Levitan, 2002). CSF influences brain development and cortical histogenesis at fetal and early posthatching stages .…”

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Embryonic cerebrospinal fluid regulates neuroepithelial survival, proliferation, and neurogenesis in chick embryos

et al. 2005

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Early in development, the behavior of neuroepithelial cells is controlled by several factors, which act in a developmentally regulated manner. Diffusible factors are secreted locally by the neuroepithelium itself, although other nearby structures may also be involved. Evidence suggests a physiological role for the cerebrospinal fluid in the development of the brain. Here, using organotypic cultures of chick embryo neuroepithelial explants from the mesencephalon, we show that the neuroepithelium in vitro is not able to self-induce cell survival, replication, and neurogenesis. We also show that the embryonic cerebrospinal fluid (E-CSF) promotes neuroepithelial stem cell survival and induces proliferation and neurogenesis in mesencephalic explants. These data strongly suggest that E-CSF is involved in the regulation of neuroepithelial cells behavior, supporting the hypothesis that this fluid plays a key role during the early development of the central nervous system.

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Apparent lability of neural tube closure in laboratory animals and humans

1999

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Neural tube defects (NTDs), a set of structural abnormalities affecting the brain, spinal cord, and the skeletal and connective tissues that protect them, are common malformations among humans and laboratory animals. The embryogenesis of the neural tube is presented to convey the complexity of the phenomenon, the multiplicity of requisite cellular and subcellular processes, and the precise timing of events that must occur for successful neural tube development. Interruption, even transitory, of any of these intricate processes or disruption of an embryo's developmental schedule can lead to an NTD. The population distribution of human NTDs demonstrates that genetic predisposition functions in susceptibility to NTDs. Data from animal studies support these concepts. NTDs are common outcomes in developmental toxicity safety assessments, occurring among control and treated groups. Numerous agents have caused increased levels of NTDs in laboratory animals, and species with shorter gestational periods appear more prone to toxicant-induced NTDs than those with longer gestations. Data from post-implantation whole embryo culture, although not predictive of human risk, are useful in studying neurulation mechanisms and in demonstrating the importance of maintaining embryonic schedules of development. We conclude that the concept that NTDs are produced by only a few toxicants that selectively target the developing nervous system is untenable. Rather, the combination of the time in gestation that an agent is applied, its dose, and its ability to disrupt critical processes in neurulation leads to NTDs. We further conclude that, because of both the relatively high prevalence and the multifactorial nature of NTDs, the mere occurrence of an NTD is insufficient for inferring that the defect was caused by an exogenous agent.

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Embryonic brain enlargement requires cerebrospinal fluid pressure

Cited by 233 publications

References 21 publications

Cdc42 deficiency causes Sonic hedgehog-independent holoprosencephaly

Cdc42 deficiency causes Sonic hedgehog-independent holoprosencephaly

Embryonic cerebrospinal fluid regulates neuroepithelial survival, proliferation, and neurogenesis in chick embryos

Apparent lability of neural tube closure in laboratory animals and humans

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