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利用者:加藤勝憲/放射状グリア細胞

 Template:Infobox cell放射状グリア細胞、または放射状グリア前駆細胞(RGP)は、大脳皮質のすべてのニューロンを産生する役割を持つ双極形前駆細胞である。RGPはまた、アストロサイトオリゴデンドロサイトなど、ある系統のグリアも産生する[1][2][3]。RGPの細胞体(体節)は、発達中の脳室系英語版の隣にある胚性脳室帯に存在する。

発生過程において、新生ニューロンは放射状グリアを足場として、放射状グリア線維に沿って移動し、最終目的地に到達する[1][4][5]。放射状グリア集団の様々な運命が考えられるにもかかわらず、クローン解析によって、ほとんどの放射状グリアが制限された、単能性または多能性の運命を持つことが証明されている。放射状グリアは、(現在までに研究された)すべての脊椎動物において、神経発生期に見られる[6]

放射状グリア」という用語は、最初に観察されたこれらの細胞の形態学的特徴、すなわち放射状の突起と、グリア細胞ファミリーのもう一つのメンバーであるアストロサイトとの類似性を指す[7]

構造

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ミュラーグリア

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ミュラーグリア英語版は放射状のグリア細胞で、成体だけでなく発達中の網膜にも存在する。大脳皮質と同様に、ミュラーグリアは基底細胞層から先端細胞層まで、網膜の全幅に及ぶ長い突起を持つ。しかし、皮質の放射状グリアとは異なり、ミュラーグリアは神経新生の最初のラウンドが起こるまでは網膜に現れない。研究によると、ミュラーグリアは傷害に反応して、容易に分裂する神経前駆細胞に分化することができる[8]

Slcla3 in Bergmann Glia

The characteristics that truly set Müller glia apart from radial glia in other areas of the brain, is their possession of optical properties. The majority of the retina is actually largely light scattering, suggesting that Müller glia serve as the main fiber responsible for the relay of light to the photoreceptors in the rear of the retina. Properties that help Müller glia achieve this function include a limited number mitochondria (which are very light scattering), as well as a specialized arrangement of internal protein filaments.[8]

Müller glia are the predominant type of macroglia in the retina, so they take on many of the supportive functions that astrocytes and oligodendrocytes usually handle in the rest of the central nervous system.[8]

バーグマングリア

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Micrograph showing Bergmann gliosis. H&E stain.

バーグマングリア(あるいは、放射状上皮細胞、ゴルジ上皮細胞、または放射状アストロサイト)は、小脳プルキンエ細胞と密接に関連している放射状グリアに由来する単極性アストロサイトである[9]。バーグマングリアは、小脳内で持続し、アストロサイトに特徴的な多くの役割を果たすことから、「特殊化アストロサイト」とも呼ばれている。 [10]バーグマングリア細胞は顆粒細胞の移動を補助し、その広範な放射状突起に沿って外顆粒層から内顆粒層へと小さなニューロンを誘導する[11][12]。 小脳の初期発達における役割の他に、バーグマングリアはシナプス刈り込みにも必要である[10]。中枢神経系傷害によって誘発されるプルキンエ細胞死の後、バーグマングリアはグリオーシスとして知られる過程で、失われたり傷ついたりした組織を置き換えるように、広範な増殖性変化を起こす[11][12]

Since bergmann glia appear to persist in the cerebellum, and perform many of the roles characteristic of astrocytes, they have also been called "specialized astrocytes."[8] Bergmann glia have multiple radial processes that extend across the molecular layer of the cerebellar cortex and terminate at the pial surface as a bulbous endfoot.[13] Bergmann glial cells assist with the migration of granule cells, guiding the small neurons from the external granular layer down to the internal granular layer along their extensive radial processes.[14][15] Besides their role in early development of the cerebellum, Bergmann glia are also required for synaptic pruning.

Development

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Radial glial cells originate from the transformation of neuroepithelial cells that form the neural plate during neurogenesis in early embryonic development.[7][8][16] This process is mediated through the down-regulation of epithelium-related protein expression (such as tight junctions) and an up-regulation of glial-specific features such as glycogen granules, the astrocyte glutamate aspartate transporter (GLAST), the intermediate filament vimentin, and, in some instances, including humans, glial fibrillary acidic protein (GFAP).[6]

After this transition, radial glia retain many of the original characteristics of neuroepithelial cells including: their apical-basal polarity, their position along the lateral ventricles of the developing cortex, and the phasic migration of their nuclei depending on their location with the cell cycle (termed “interkinetic nuclear migration”).[8][17][18]

Function

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Progenitors

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Interneuron-radial glial interactions in the developing cerebral cortex

Radial glia are now recognized as key progenitor cells in the developing nervous system. During the late stages of neurogenesis, radial glial cells divide asymmetrically in the ventricular zone, generating a new radial glial cell, as well as a postmitotic neuron or an intermediate progenitor (IPC) daughter cell. Intermediate progenitor cells then divide symmetrically in the subventricular zone to generate neurons.[17] Local environmental cues such as Notch and fibroblast growth factor (FGF) signaling, developmental period, and differing abilities of radial glia to respond to environmental cues have all been shown to influence the type of radial glia and radial glia-derived daughter cells that will be produced. FGF and Notch signaling regulate the proliferation of radial glia and the rate of neurogenesis, which affects the surface area expansion of the cerebral cortex and its ability to form surface convolutions known as gyri (see gyrification).[8][19][20] Radial glial cells show high levels of calcium transient activity, which is transmitted between RGCs in the ventricular zone and along the radial fibers bidirectionally to/from the cortical plate.[21][22] The calcium activity is thought to promote RGC proliferation and could be involved in radial communication before synapses are present in the brain. Additionally, recent evidence suggests that cues from the external sensory environment can also influence the proliferation and neural differentiation of radial glia.[8][23]

At the conclusion of cortical development, most radial glia lose their attachment to the ventricles, and migrate towards the surface of the cortex, where, in mammals, most will become astrocytes during the process of gliogenesis.[17]

While it has been suggested that radial glia most likely give rise to oligodendrocytes, through the generation of oligodendrocyte progenitor cells (OPCs), and OPCs can be generated from radial glial cells in vitro, more evidence is yet needed to conclude whether this process also occurs in the developing brain.[17][24]

Recently, radial glia that exclusively generate upper-layer cortical neurons have also been discovered.[7] Since upper cortical layers have expanded greatly in recent evolution, and are associated with higher-level information processing and thinking, radial glia have been implicated as important mediators of brain evolution.[25]

Migration Pattern

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The best characterized and first widely accepted function of radial glia is their role as scaffolds for neuronal migration in the cerebral and cerebellar cortexes. This role can be easily visualized using the electron microscope or high-resolution time-lapse microscopy, through which neurons can be seen tightly wrapped around radial glia as they travel upwards through the cortex.[7] Additional evidence suggests that many neurons may move between neighboring radial glial fibers during migration.[8]

While excitatory neuronal migration is largely radial, inhibitory, GABAergic neurons have been shown to undergo tangential migration. Tangentially migrating neurons also appear to initiate contact with radial glial fibers in the developing cortex of ferrets, implicating radial glial cells in both of these forms of migration.[8]

As radial glia seem to differentiate late in spinal cord development, near the onset of gliogenesis, it is unclear whether they are involved in spinal cord neurogenesis or migration.[7]

Compartmentalization

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Radial glia have also been implicated in forming boundaries between different axonal tracts and white matter areas of the brain.[7][26]

Clinical significance

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As radial glia serve as the primary neural and glial progenitors in the brain, as well as being crucial for proper neuronal migration, defects in radial glial function can have profound effects in the development of the nervous system.

Mutations in either Lis1 or Nde1, essential proteins for radial glial differentiation and stabilization, cause the associated neurodevelopmental diseases Lissencephaly and microlissencephaly (which literally translate to “smooth brain”). Patients with these diseases are characterized by a lack of cortical folds (sulci and gyri) and reduced brain volume. Extreme cases of Lissencephaly cause death a few months after birth, while patients with milder forms may experience mental retardation, difficulty balancing, motor and speech deficits, and epilepsy.[7]

Death of neural progenitor cells has recently been linked the mosquito-borne virus, Zika.[27] Epidemiological evidence indicates infection of the embryo within the first two trimesters of pregnancy has potential to cause fetal birth defects and microcephaly,[28] possibly due to the death of progenitor cells. Further, mutations in microcephaly associated genes which encode proteins such as WDR62 can lead to radial glial depletion during brain development which ultimately leads to a smaller brain size and mental disabilities. [29]

History

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Camillo Golgi, using his silver staining technique (later deemed the Golgi method), first described radially oriented cells spanning from the central canal to the outer surface of the embryonic chick spinal cord, in 1885.[30]

Using the Golgi method, Giuseppe Magini then studied the mammalian fetal cerebral cortex in 1888, confirming the similar presence of elongated radial cells in the cortex (also described by Kölliker just before him), and observing “various varicosities or swellings” on the radial fibers. Intrigued, Magini also observed that the size and number of these varicosities increased later in development, and were absent in the adult nervous system. Based on these findings, Magini then hypothesized that these varicosities could be developing neurons. Using a combination Golgi and hematoxylin staining method, Magini was able to identify these varicosities as cells, some of which were very closely associated with the radial fibers.[30]

Additional early works that were important in elucidating the identity and function of radial glia, were completed by Ramón y Cajal, who first suggested that the radial cells were a type of glia through their similarities to astrocytes;[7] and Wilhelm His, who also proposed the idea that growing axons may use radial cells for orientation and guidance during development.[30]

Despite the initial period of interest in radial glia, little additional information was learned about these cells until the electron microscope and immunohistochemistry became available some 60 years later.[30]

関連項目

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List of distinct cell types in the adult human body

脚注・参考文献

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  1. ^ a b “Evolution of the neocortex: a perspective from developmental biology”. Nature Reviews. Neuroscience 10 (10): 724–35. (October 2009). doi:10.1038/nrn2719. PMC 2913577. PMID 19763105. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2913577/. 
  2. ^ Beattie, R; Hippenmeyer, S (December 2017). “Mechanisms of radial glia progenitor cell lineage progression.”. FEBS Letters 591 (24): 3993–4008. doi:10.1002/1873-3468.12906. PMC 5765500. PMID 29121403. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5765500/. 
  3. ^ “Neurons derived from radial glial cells establish radial units in neocortex”. Nature 409 (6821): 714–20. (February 2001). Bibcode2001Natur.409..714N. doi:10.1038/35055553. PMID 11217860. 
  4. ^ “Mode of cell migration to the superficial layers of fetal monkey neocortex”. The Journal of Comparative Neurology 145 (1): 61–83. (May 1972). doi:10.1002/cne.901450105. PMID 4624784. 
  5. ^ “Conservation of neural progenitor identity and the emergence of neocortical neuronal diversity”. Seminars in Cell and Developmental Biology 118 (118): 4–13. (October 2021). doi:10.1016/j.semcdb.2021.05.024. PMID 34083116. https://www.sciencedirect.com/science/article/abs/pii/S1084952121001336. 
  6. ^ a b “Radial glia and neural stem cells”. Cell and Tissue Research 331 (1): 165–78. (January 2008). doi:10.1007/s00441-007-0481-8. PMID 17846796. 
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  8. ^ a b c d e f g h i j “Radial glia: progenitor, pathway, and partner”. The Neuroscientist 17 (3): 288–302. (June 2011). doi:10.1177/1073858410385870. PMID 21558559. 
  9. ^ Verkhratsky, Alexei; Butt, Arthur M. (2013). Glial Physiology and Pathophysiology. John Wiley and Sons, Inc.. ISBN 9780470978535 
  10. ^ Bergmann Glial Cell” (14 Oct 2011). 10 September 2014閲覧。
  11. ^ “Astrogliosis”. Cold Spring Harbor Perspectives in Biology 7 (2): a020420. (November 2014). doi:10.1101/cshperspect.a020420. PMC 4315924. PMID 25380660. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4315924/. 
  12. ^ Catherine., Haberland (2007). Clinical neuropathology : text and color atlas. New York: Demos. ISBN 9781934559529. OCLC 166267295 
  13. ^ “The monolayer formation of Bergmann glial cells is regulated by Notch/RBP-J signaling”. Developmental Biology 311 (1): 238–50. (November 2007). doi:10.1016/j.ydbio.2007.08.042. PMID 17915208. 
  14. ^ Rubenstein, John; Rakic, Pasko (2013). Cellular Migration and Formation of Neuronal Connections: Comprehensive Developmental Neuroscience. Elsevier Science and Technology. ISBN 9780123972668 
  15. ^ Sanes, Dan H.; Reh, Thomas A.; Harris, William A. (2005). Development of the Nervous System. Elsevier Science and Technology. ISBN 9780126186215 
  16. ^ “Conservation of neural progenitor identity and the emergence of neocortical neuronal diversity”. Seminars in Cell and Developmental Biology 118 (118): 4–13. (October 2021). doi:10.1016/j.semcdb.2021.05.024. PMID 34083116. https://www.sciencedirect.com/science/article/abs/pii/S1084952121001336. 
  17. ^ a b c d “The glial nature of embryonic and adult neural stem cells”. Annual Review of Neuroscience 32: 149–84. (2009). doi:10.1146/annurev.neuro.051508.135600. PMC 3086722. PMID 19555289. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3086722/. 
  18. ^ “Conservation of neural progenitor identity and the emergence of neocortical neuronal diversity”. Seminars in Cell and Developmental Biology 118 (118): 4–13. (October 2021). doi:10.1016/j.semcdb.2021.05.024. PMID 34083116. https://www.sciencedirect.com/science/article/abs/pii/S1084952121001336. 
  19. ^ “FGF signaling expands embryonic cortical surface area by regulating Notch-dependent neurogenesis”. The Journal of Neuroscience 31 (43): 15604–17. (October 2011). doi:10.1523/jneurosci.4439-11.2011. PMC 3235689. PMID 22031906. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3235689/. 
  20. ^ “Cortical gyrification induced by fibroblast growth factor 2 in the mouse brain”. The Journal of Neuroscience 33 (26): 10802–14. (June 2013). doi:10.1523/jneurosci.3621-12.2013. PMC 3693057. PMID 23804101. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3693057/. 
  21. ^ “Calcium waves propagate through radial glial cells and modulate proliferation in the developing neocortex”. Neuron 43 (5): 647–61. (September 2004). doi:10.1016/j.neuron.2004.08.015. PMID 15339647. 
  22. ^ “Bidirectional radial Ca(2+) activity regulates neurogenesis and migration during early cortical column formation”. Science Advances 2 (2): e1501733. (February 2016). Bibcode2016SciA....2E1733R. doi:10.1126/sciadv.1501733. PMC 4771444. PMID 26933693. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4771444/. 
  23. ^ “Visual activity regulates neural progenitor cells in developing xenopus CNS through musashi1”. Neuron 68 (3): 442–55. (November 2010). doi:10.1016/j.neuron.2010.09.028. PMC 3005332. PMID 21040846. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3005332/. 
  24. ^ “Human fetal radial glia cells generate oligodendrocytes in vitro”. Glia 57 (5): 490–8. (April 2009). doi:10.1002/glia.20775. PMC 2644732. PMID 18814269. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2644732/. 
  25. ^ Scripps Research Neuroscientists Find Brain Stem Cells that May Be Responsible for Higher Functions, Bigger Brains”. Scripps Research Institute. 1 March 2014閲覧。
  26. ^ “Glial boundaries in the developing nervous system”. Annual Review of Neuroscience 16: 445–70. (1993). doi:10.1146/annurev.ne.16.030193.002305. PMID 8460899. 
  27. ^ “Zika Virus Infects Human Cortical Neural Progenitors and Attenuates Their Growth”. Cell Stem Cell 18 (5): 587–90. (May 2016). doi:10.1016/j.stem.2016.02.016. PMC 5299540. PMID 26952870. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5299540/. 
  28. ^ “Zika Virus Associated with Microcephaly”. The New England Journal of Medicine 374 (10): 951–8. (March 2016). doi:10.1056/NEJMoa1600651. PMID 26862926. 
  29. ^ “The association of microcephaly protein WDR62 with CPAP/IFT88 is required for cilia formation and neocortical development”. Human Molecular Genetics 29 (2): 248–263. (January 2020). doi:10.1093/hmg/ddz281. PMID 31816041. 
  30. ^ a b c d “The history of radial glia”. Brain Research Bulletin 49 (5): 305–15. (July 1999). doi:10.1016/s0361-9230(99)00065-9. PMID 10452351. 

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