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Radial glial cells ( RGCs), or radial glial progenitor cells ( RGPs), are Bipolar neuron-shaped that are responsible for producing all of the in the cerebral cortex. RGPs also produce certain lineages of glia, including and . Their Cell body (somata) reside in the embryonic ventricular zone, which lies next to the developing ventricular system.
During development, neuroblast use radial glia as scaffolds, traveling along the radial glial in order to reach their final destinations. Despite the various possible fates of the radial glial population, it has been demonstrated through clonal analysis that most radial glia have restricted, unipotent or multipotent, fates. Radial glia can be found during the Neurogenesis phase in all vertebrates (studied to date).
The term "radial glia" refers to the morphological characteristics of these cells that were first observed: namely, their radial processes and their similarity to , another member of the glial cell family.
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.
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.
After this transition, radial glia retain many of the original characteristics of neuroepithelial cells including: their Cell polarity, their position along the lateral ventricles of the developing cortex, and the phasic migration of their Cell nucleus depending on their location with the cell cycle (termed "interkinetic nuclear migration").
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.
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.
Recently, radial glia that exclusively generate upper-layer cortical neurons have also been discovered. 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.
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.
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.
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 gyrus) 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.
Death of neural progenitor cells has recently been linked the mosquito-borne virus, Zika virus. Epidemiological evidence indicates infection of the embryo within the first two trimesters of pregnancy has potential to cause fetal birth defects and microcephaly, 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.
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.
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; and Wilhelm His, who also proposed the idea that growing axons may use radial cells for orientation and guidance during development.
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.
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