Talk:Neural System - Glial Development

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On this website the Discussion Tab or "talk pages" for a topic has been used for several purposes: References - recent and historic that relates to the topic Additional topic information - currently prepared in draft format Links - to related webpages Topic page - an edit history as used on other Wiki sites Lecture/Practical - student feedback Student Projects - online project discussions. Links: Pubmed Most Recent | Reference Tutorial | Journal Searches Glossary Links Glossary: A | B | C | D | E | F | G | H | I | J | K | L | M | N | O | P | Q | R | S | T | U | V | W | X | Y | Z | Numbers | Symbols | Term Link Cite this page: Hill, M.A. (2024, April 19) Embryology Neural System - Glial Development. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Talk:Neural_System_-_Glial_Development

2014

Radial glial cells: key organisers in CNS development

Int J Biochem Cell Biol. 2014 Jan;46:76-9. doi: 10.1016/j.biocel.2013.11.013. Epub 2013 Nov 21.

Barry DS1, Pakan JM2, McDermott KW2.

Abstract Radial glia are elongated bipolar cells present in the CNS during development. Our understanding of the unique roles these cells play has significantly expanded in the last decade. Historically, radial glial cells were primarily thought to provide an architectural framework for neuronal migration. Recent research reveals that radial glia play a more dynamic and integrated role in the development of the brain and spinal cord. They represent a major progenitor pool during early development and can give rise to a small population of multipotent cells in neurogenic niches of the adult CNS. Radial glial cells are a heterogeneous population, with divergent and often poorly understood roles across different brain and spinal cord regions during development; this heterogeneity extends to specialised adult subtypes, such as tanycytes, Müller glial cells and Bergman glial cells which possess morphological similarities to radial glial but play distinct functional roles in the CNS. Copyright © 2013 Elsevier Ltd. All rights reserved. KEYWORDS: Glioma; Neurodevelopment; Neuronal migration; Radial glia PMID 24269781

Stem cell factor Sox2 and its close relative Sox3 have differentiation functions in oligodendrocytes

Development. 2014 Jan;141(1):39-50. doi: 10.1242/dev.098418. Epub 2013 Nov 20.

Hoffmann SA1, Hos D, Küspert M, Lang RA, Lovell-Badge R, Wegner M, Reiprich S.

Abstract

Neural precursor cells of the ventricular zone give rise to all neurons and glia of the central nervous system and rely for maintenance of their precursor characteristics on the closely related SoxB1 transcription factors Sox1, Sox2 and Sox3. We show in mouse spinal cord that, whereas SoxB1 proteins are usually downregulated upon neuronal specification, they continue to be expressed in glial precursors. In the oligodendrocyte lineage, Sox2 and Sox3 remain present into the early phases of terminal differentiation. Surprisingly, their deletion does not alter precursor characteristics but interferes with proper differentiation. Although a direct influence on myelin gene expression may be part of their function, we provide evidence for another mode of action. SoxB1 proteins promote oligodendrocyte differentiation in part by negatively controlling miR145 and thereby preventing this microRNA from inhibiting several pro-differentiation factors. This study presents one of the few cases in which SoxB1 proteins, including the stem cell factor Sox2, are associated with differentiation rather than precursor functions. KEYWORDS: Glia; High mobility group; MicroRNA; Myelin; Transcriptional control

PMID 24257626

http://dev.biologists.org/content/141/1/39.full?sid=2eb152f3-6a5b-4644-855b-f781bf928891

2010

Sox10 is required for Schwann cell identity and progression beyond the immature Schwann cell stage

J Cell Biol. 2010 May 17;189(4):701-12. Epub 2010 May 10.

Finzsch M, Schreiner S, Kichko T, Reeh P, Tamm ER, Bösl MR, Meijer D, Wegner M.

Institut für Biochemie, Emil-Fischer-Zentrum, Universität Erlangen-Nürnberg, 91054 Erlangen, Germany.

Abstract Mutations in the transcription factor SOX10 cause neurocristopathies, including Waardenburg-Hirschsprung syndrome and peripheral neuropathies in humans. This is partly attributed to a requirement for Sox10 in early neural crest for survival, maintenance of pluripotency, and specification to several cell lineages, including peripheral glia. As a consequence, peripheral glia are absent in Sox10-deficient mice. Intriguingly, Sox10 continues to be expressed in these cells after specification. To analyze glial functions after specification, we specifically deleted Sox10 in immature Schwann cells by conditional mutagenesis. Mutant mice died from peripheral neuropathy before the seventh postnatal week. Nerve alterations included a thinned perineurial sheath, increased lipid and collagen deposition, and a dramatically altered cellular composition. Nerve conduction was also grossly aberrant, and neither myelinating nor nonmyelinating Schwann cells formed. Instead, axons of different sizes remained unsorted in large bundles. Schwann cells failed to develop beyond the immature stage and were unable to maintain identity. Thus, our study identifies a novel cause for peripheral neuropathies in patients with SOX10 mutations.

PMID 20457761

http://www.ncbi.nlm.nih.gov/pubmed/20457761

2009

Growth of the human corpus callosum: modular and laminar morphogenetic zones

Front Neuroanat. 2009;3:6. Epub 2009 Jun 9.

Jovanov-Milosević N, Culjat M, Kostović I.

Croatian Institute for Brain Research, School of Medicine, University of Zagreb Zagreb, Croatia. Abstract The purpose of this focused review is to present and discuss recent data on the changing organization of cerebral midline structures that support the growth and development of the largest commissure in humans, the corpus callosum. We will put an emphasis on the callosal growth during the period between 20 and 45 postconceptual weeks (PCW) and focus on the advantages of a correlated histological/magnetic resonance imaging (MRI) approach. The midline structures that mediate development of the corpus callosum in rodents, also mediate its early growth in humans. However, later phases of callosal growth in humans show additional medial transient structures: grooves made up of callosal septa and the subcallosal zone. These modular (septa) and laminar (subcallosal zone) structures enable the growth of axons along the ventral callosal tier after 18 PCW, during the rapid increase in size of the callosal midsagittal cross-section area. Glial fibrillary acidic protein positive cells, neurons, guidance molecule semaphorin3A in cells and extracellular matrix (ECM), and chondroitin sulfate proteoglycan in the ECM have been identified along the ventral callosal tier in the protruding septa and subcallosal zone. Postmortem MRI at 3 T can demonstrate transient structures based on higher water content in ECM, and give us the possibility to follow the growth of the corpus callosum in vivo, due to the characteristic MR signal. Knowledge about structural properties of midline morphogenetic structures may facilitate analysis of the development of interhemispheric connections in the normal and abnormal fetal human brain.

PMID: 19562029

http://www.ncbi.nlm.nih.gov/pubmed/19562029

http://www.frontiersin.org/neuroanatomy/10.3389/neuro.05.006.2009/full

Cell migration in the normal and pathological postnatal mammalian brain

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2728466/?tool=pubmed

http://www.ncbi.nlm.nih.gov/pubmed/19428961

EMs

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2592840/?tool=pubmed

Integrin-mediated axoglial interactions initiate myelination in the central nervous system

J Cell Biol. 2009 May 18;185(4):699-712.

Câmara J, Wang Z, Nunes-Fonseca C, Friedman HC, Grove M, Sherman DL, Komiyama NH, Grant SG, Brophy PJ, Peterson A, ffrench-Constant C.

Department of Pathology, University of Cambridge, Cambridge CB2 1QP, England, UK. Abstract

All but the smallest-diameter axons in the central nervous system are myelinated, but the signals that initiate myelination are unknown. Our prior work has shown that integrin signaling forms part of the cell-cell interactions that ensure only those oligodendrocytes contacting axons survive. Here, therefore, we have asked whether integrins regulate the interactions that lead to myelination. Using homologous recombination to insert a single-copy transgene into the hypoxanthine phosphoribosyl transferase (hprt) locus, we find that mice expressing a dominant-negative beta1 integrin in myelinating oligodendrocytes require a larger axon diameter to initiate timely myelination. Mice with a conditional deletion of focal adhesion kinase (a signaling molecule activated by integrins) exhibit a similar phenotype. Conversely, transgenic mice expressing dominant-negative beta3 integrin in oligodendrocytes display no myelination abnormalities. We conclude that beta1 integrin plays a key role in the axoglial interactions that sense axon size and initiate myelination, such that loss of integrin signaling leads to a delay in myelination of small-diameter axons.

PMID: 19451276

http://www.ncbi.nlm.nih.gov/pubmed/19451276

The contributions of Santiago Ramón y Cajal to cancer research — 100 years on

http://www.nature.com/nrc/journal/v5/n11/full/nrc1741.html

2005

J Anat. 2005 Sep;207(3):241-50. Role of radial glia in cytogenesis, patterning and boundary formation in the developing spinal cord. McDermott KW1, Barry DS, McMahon SS. Author information Abstract Radial glial fibres provide a transient scaffold and impose constraints in the developing central nervous system (CNS) that facilitate cell migration and axon growth. Recent reports have raised doubts about the distinction between radial glia and precursor cells by demonstrating that radial glia are themselves neuronal progenitor cells in the developing cortex, indicating a dual role for radial glia in both neurogenesis and migration guidance. Radial glia shift toward exclusive generation of astrocytes after neurogenesis has ceased. Radial progenitor cell differentiation and lineage relationships in CNS development are complex processes depending on genetic programming, cell-cell interaction and microenvironmental factors. In the spinal cord, radial cells that arise directly from the neuroepithelium have been identified. At least in the spinal cord, these radial cells appear to be the precursors to radial glia. It remains unknown whether radial glial cells or their precursors, the radial cells, or both can give rise to neurons in the spinal cord. Radial glial cells are also important in regulating the axon out-growth and pathfinding processes that occur during white matter patterning of the developing spinal cord. PMID 16185248

2008

Progressive loss of PAX6, TBR2, NEUROD and TBR1 mRNA gradients correlates with translocation of EMX2 to the cortical plate during human cortical development

Eur J Neurosci. 2008 Oct;28(8):1449-56.

Bayatti N, Sarma S, Shaw C, Eyre JA, Vouyiouklis DA, Lindsay S, Clowry GJ.

Institute of Neuroscience, Newcastle University, Newcastle-upon-Tyne, UK. Abstract The transcription factors Emx2 and Pax6 are expressed in the proliferating zones of the developing rodent neocortex, and gradients of expression interact in specifying caudal and rostral identities. Pax6 is also involved in corticoneurogenesis, being expressed by radial glial progenitors that give rise to cells that also sequentially express Tbr2, NeuroD and Tbr1, genes temporally downstream of Pax6. In this study, using in situ hybridization, we analysed the expression of EMX2, PAX6, TBR2, NEUROD and TBR1 mRNA in the developing human cortex between 8 and 12 postconceptional weeks (PCW). EMX2 mRNA was expressed in the ventricular (VZ) and subventricular zones (SVZ), but also in the cortical plate, unlike in the rodent. However, gradients of expression were similar to that of the rodent at all ages studied. PAX6 mRNA expression was limited to the VZ and SVZ. At 8 PCW, PAX6 was highly expressed rostrally but less so caudally, as has been seen in the rodent, however this gradient disappeared early in corticogenesis, by 9 PCW. There was less restricted compartment-specific expression of TBR2, NEUROD and TBR1 mRNA than in the rodent, where the gradients of expression were similar to that of PAX6 prior to 9 PCW. The gradient disappeared for TBR2 by 10 PCW, and for NEUROD and TBR1 by 12 PCW. These data support recent reports that EMX2 but not PAX6 is more directly involved in arealization, highlighting that analysis of human development allows better spatio-temporal resolution than studies in rodents.

http://www.ncbi.nlm.nih.gov/pubmed/18973570

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http://www.ncbi.nlm.nih.gov/pubmed/19896829

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2845925/?tool=pubmed

2005

Role of radial glia in cytogenesis, patterning and boundary formation in the developing spinal cord

J Anat. 2005 Sep;207(3):241-50.

McDermott KW1, Barry DS, McMahon SS.

Abstract

Radial glial fibres provide a transient scaffold and impose constraints in the developing central nervous system (CNS) that facilitate cell migration and axon growth. Recent reports have raised doubts about the distinction between radial glia and precursor cells by demonstrating that radial glia are themselves neuronal progenitor cells in the developing cortex, indicating a dual role for radial glia in both neurogenesis and migration guidance. Radial glia shift toward exclusive generation of astrocytes after neurogenesis has ceased. Radial progenitor cell differentiation and lineage relationships in CNS development are complex processes depending on genetic programming, cell-cell interaction and microenvironmental factors. In the spinal cord, radial cells that arise directly from the neuroepithelium have been identified. At least in the spinal cord, these radial cells appear to be the precursors to radial glia. It remains unknown whether radial glial cells or their precursors, the radial cells, or both can give rise to neurons in the spinal cord. Radial glial cells are also important in regulating the axon out-growth and pathfinding processes that occur during white matter patterning of the developing spinal cord. PMID: 16185248

2002

Radial glia: multi-purpose cells for vertebrate brain development

Trends Neurosci. 2002 May;25(5):235-8.

Campbell K1, Götz M.

Abstract

Radial glia are specialized cells in the developing nervous system of all vertebrates, and are characterized by long radial processes. These processes facilitate the best known function of radial glia: guiding the radial migration of newborn neurons from the ventricular zone to the mantle regions. Recent data indicate further important roles for these cells as ubiquitous precursors that generate neurons and glia, and as key elements in patterning and region-specific differentiation of the CNS. Thus, from being regarded mainly as support cells, radial glia have emerged as multi-purpose cells involved in most aspects of brain development. PMID 11972958

1994

Patterns of glial development in the human foetal spinal cord during the late first and second trimester

J Neurocytol. 1994 Jun;23(6):343-53.

Weidenheim KM, Epshteyn I, Rashbaum WK, Lyman WD.

Department of Pathology (Neuropathology), Albert Einstein College of Medicine, Bronx, New York. Abstract

Although the presence of radial glia, astrocytes, oligodendrocytes and microglia has been reported in the human foetal spinal cord by ten gestational weeks, neuroanatomic studies employing molecular probes that describe the interrelated development of these cells from the late first trimester through the late second trimester are few. In this study, immunocytochemical methods using antibodies to vimentin and glial fibrillary acidic protein were used to identify radial glial and/or astrocytes. An antibody to myelin basic protein was used for oligodendrocytes and myelin; and, an antibody to phosphorylated high and medium molecular weight neurofilaments identified axons. Lectin histochemistry using Ricinus communis agglutinin-I was employed to identify microglia. Vibratome sections from 35 human foetal spinal cord ranging in age from 9-20 gestation weeks were studied. By 12 gestational weeks, vimentin-positive radial glia were present at all three levels of the spinal cord. Their processes were easily identified in the dorsal two-thirds of cord sections, and reaction product for vimentin was more intense at cervical and thoracic levels than lumbosacral sections. By 15 gestational weeks, vimentin-positive processes were radially arranged in the white matter. At this time, glial fibrillary acidic protein-positive astrocytes were more obvious in both the anterior and anterolateral funiculi than in the dorsal funiculus, and the same rostral to caudal gradient was seen for glial fibrillary acidic protein as it was for vimentin. Myelin basic protein expression followed similar temporal and spatial patterns. Ricinus communis agglutinin-I labelling revealed more microglia in the white matter than in grey matter throughout the spinal cord from 10-20 gestational weeks. By 20 gestational weeks, the gradients of glial fibrillary acidic protein and vimentin expression were more difficult to discern. White matter contained more microglia than grey matter. These results suggest that astrocytes as well as oligodendrocytes follow anterior-to-posterior and rostral-to-caudal developmental patterns in the human foetus during middle trimester development.

12 gestational weeks - vimentin-positive radial glia 15 gestational weeks - vimentin-positive processes were radially arranged in the white matter. 20 gestational weeks - gradients of glial fibrillary acidic protein and vimentin expression were more difficult to discern.

PMID: 7522270

1999

Microglia derive from progenitors, originating from the yolk sac, and which proliferate in the brain

Brain Res Dev Brain Res. 1999 Nov 18;117(2):145-52.

Alliot F1, Godin I, Pessac B.

Abstract

Microglia, the resident CNS macrophages, represent about 10% of the adult brain cell population. Although described a long time ago, their origin and developmental lineage is still debated. While del Rio-Hortega suggested that microglia originate from meningeal macrophages penetrating the brain during embryonic development, many authors claim that brain parenchymal microglia derive from circulating blood monocytes originating from bone marrow. We have previously reported that the late embryonic and adult mouse brain parenchyma contains potential microglial progenitors [F. Alliot, E. Lecain, B. Grima, B. Pessac, Microglial progenitors with a high proliferative capacity in the embryonic and the adult mouse brain, Proc. Natl. Acad. Sci. U.S.A. 88 (1991) 1541-1545]. We now report that they can be detected in the brain rudiment from embryonic day 8, after their appearance in the yolk sac and that their number increases until late gestation. We also show that microglia appear during embryonic development and that their number increases steadily during the first two postnatal weeks, when about 95% of microglia are born. Finally, the main finding of this study is that microglia is the result of in situ proliferation, as shown by the high proportion of parenchymal microglial cells that express PCNA, a marker of cell multiplication, in embryonic and postnatal brain. Taken together, our data support the hypothesis that terminally differentiated brain parenchymal microglia are derived from cells originating from the yolk sac whose progeny actively proliferates in situ during development.

PMID 10567732

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