Information

17.25: Glial Cells - Biology

17.25: Glial Cells - Biology



We are searching data for your request:

Forums and discussions:
Manuals and reference books:
Data from registers:
Wait the end of the search in all databases.
Upon completion, a link will appear to access the found materials.

While glia are often thought of as the supporting cast of the nervous system, the number of glial cells in the brain actually outnumbers the number of neurons by a factor of ten. When glia do not function properly, the result can be disastrous—most brain tumors are caused by mutations in glia.

Types of Glia

There are several different types of glia with different functions, two of which are shown in Figure 1.

Astrocytes, shown in Figure 2a make contact with both capillaries and neurons in the CNS. They provide nutrients and other substances to neurons, regulate the concentrations of ions and chemicals in the extracellular fluid, and provide structural support for synapses. Astrocytes also form the blood-brain barrier—a structure that blocks entrance of toxic substances into the brain. Astrocytes, in particular, have been shown through calcium imaging experiments to become active in response to nerve activity, transmit calcium waves between astrocytes, and modulate the activity of surrounding synapses.

Satellite glia provide nutrients and structural support for neurons in the PNS. Microglia scavenge and degrade dead cells and protect the brain from invading microorganisms. Oligodendrocytes, shown in Figure 2b form myelin sheaths around axons in the CNS. One axon can be myelinated by several oligodendrocytes, and one oligodendrocyte can provide myelin for multiple neurons. This is distinctive from the PNS where a single Schwann cell provides myelin for only one axon as the entire Schwann cell surrounds the axon. Radial glia serve as scaffolds for developing neurons as they migrate to their end destinations. Ependymal cells line fluid-filled ventricles of the brain and the central canal of the spinal cord. They are involved in the production of cerebrospinal fluid, which serves as a cushion for the brain, moves the fluid between the spinal cord and the brain, and is a component of the choroid plexus.


Glial Cell Biology

The fruit fly Drosophila melanogaster is emerging as a major invertebrate model for studies of glial cell development and function. Interest in the fly as a model for glial cell biology stems from the combination of its relatively sophisticated nervous system and its access experimentally through robust genetics. Both larval and adult Drosophila have complex compartmentalized brains which house neurons with electrophysiological and functional properties quite similar to mammalian neuronal cell types ( Freeman and Doherty, 2006 ). Fly neural circuits encode a diverse behavioral repertoire, many of the neurons driving these behaviors have been defined in exquisite detail and can be easily studied morphologically or electrophysiologically, and a number of neural circuits are known to exhibit plasticity at either the electrophysiological or behavioral level ( Zhang et al., 2010 ). Importantly, the fly nervous system (like many other ‘higher’ invertebrates) houses glial subtypes with striking morphological and molecular similarities to a number of subtypes of mammalian glia, and it therefore seems likely that studies of fly glial studies will be instructive in understanding mammalian glial biology ( Edwards and Meinertzhagen, 2010 Freeman and Doherty, 2006 ). Finally, there is a vast array of molecular genetic tools available in Drosophila with which to manipulate individual or populations of glial cells and single genes in vivo, so one can incisively address glial gene function in the intact organism, and (as with C. elegans) it is highly feasible to perform powerful forward genetic screens to address either broad or very specific questions in glial cell biology.


Glial cell types and their functions

Glial cells are usually classified into two large groups, macroglial cells or macroglia , which have an ectodermal (neural) origin, and microglia , which have mesodermal origin. Both types are present in both the central and peripheral nervous systems.

Macroglia of the CNS

In the central nervous system (CNS) several types of glial cells can be found, among the most important we find:

Astrocyte function

They also regulate the conditions of the external chemical microenvironment of neurons, removing excess potassium, recycling neurotransmitters and regulating blood vasoconstriction and vasodilation. They also appear to have an inhibitory role in neuronal circuits through the detection of changes in the extracellular calcium concentration.

The recycling of neurotransmitters, removing them from the synaptic space, has an important role in the regulation of synaptic function and in preventing the reaching of toxic concentrations of some neurotransmitters, for example glutamate.

Oligodendrocytes

Oligodendrocytes are cells with projections that cover the axons of neurons in the central nervous system and form the myelin sheath . The myelin sheath electrically insulates the axons and allows for more efficient nerve transmission.

Radial glial cells

During embryonic development, radial cells act as progenitors of neurons and at the same time guide the migration of new neurons. In adults they remain as specialized glial cells in some areas, such as the retina and cerebellum . In the cerebellum, Bergmann’s glia regulates synaptic plasticity in the retina, Müller cells are the only macroglia and perform functions similar to astrocytes and oligodendrocytes of the CNS.

Others

  • Pituitcytes : specialized glial cells similar to astrocytes that appear in the neurohypophysis or posterior pituitary. Its main function is the storage and release of pituitary hormones . The pituicytes surround the terminal axons and regulate the release of these hormones.
  • Tanicytes : are a type of specialized ependymocytes that appear in the third cerebral ventricle and in the lower part of the fourth ventricle. They appear to be involved in the release of GnRH (gonadotropin-releasing hormone) by neurons in the hypothalamus.

Macroglia of the SNP

Fewer glial cells appear in the peripheral nervous system and are usually differentiated cells from the macroglia of the central nervous system. Some of the most important are the following:

  • Neurolemocytes : Also called Schwann cells . They have a similar function to oligodendrocytes of the CNS and form the myelin sheath in the axons of the PNS. They have phagocytic activity eliminating cellular debris and also appear to guide the growth of neuronal axons.
  • Satellite cells : they are small cells that surround the neuronal bodies in sensory, sympathetic and parasympathetic ganglia . They have an important role in the regulation of the microenvironment in these ganglia and are very sensitive to lesions and inflammatory processes They seem to be involved in various pathological processes that occur with chronic pain.
  • Enteric glial cells : These are glial cells found in the enteric nervous system , the subdivision of the autonomic nervous system that is responsible for directly controlling the digestive system.

Microglia

Microglial cells are not really considered glial cells, since they do not have the same embryological origin as the rest of the cells of the nervous system . Microglial cells are specialized macrophages that form in the bone marrow and migrate to the nervous system. They are present only in the central nervous system .

Microglial cells have phagocytic activity and are the cells that regulate the immune system response in the central nervous system by acting as antigen-presenting cells . Microglial cell deficiency is seen in several diseases that affect the central nervous system, such as Alzheimer’s, Parkinson’s, and amyotrophic lateral sclerosis.


Glial cells help mitigate neurological damage in Huntington's disease

Confocal microscopy image showing the striatum in a mouse model of Huntington’s Disease. The astrocytes are visualized in green and cell nuclei in blue. Credit: J. Botas/eLife

The brain is not a passive recipient of injury or disease. Research has shown that when neurons die and disrupt the natural flow of information they maintain with other neurons, the brain compensates by redirecting communications through other neuronal networks. This adjustment or rewiring continues until the damage goes beyond compensation.

This process of adjustment, a result of the brain's plasticity, or its ability to change or reorganize neural networks, occurs in neurodegenerative conditions such as Alzheimer's, Parkinson's and Huntington's disease (HD). As the conditions progress, many genes change the way they are normally expressed, turning some genes up and others down. The challenge for researchers like Dr. Juan Botas, who studies HD, has been to determine which of the gene expression changes are involved in causing the disease and which ones help mitigate the damage, as this may be critical for designing effective therapeutic interventions.

In his lab at Baylor College of Medicine, Botas and his colleagues look to understand what causes the loss of communication or synapses between neurons in HD. Up until now, research has focused on neurons because the normal huntingtin gene, whose mutation causes the condition, contributes to maintaining healthy neuronal communication. In the current work, the researchers looked into synapses loss in HD from a different perspective.

Focusing on glia to understand Huntington's disease

The mutated huntingtin gene is not only present in neurons, but in all the cells in the body, opening the possibility that other cell types also could be involved in the condition.

"In this study we focused on glia cells, which are a type of brain cell that is just as important as neurons to neuronal communication," said Botas, professor of molecular and human genetics and of molecular and cellular biology at Baylor and a member of the Jan and Dan Duncan Neurological Research Institute at Texas Children's Hospital.

"We thought that glia might be playing a role in either contributing or compensating for the damage observed in Huntington's disease."

Initially thought to be little more than housekeeping cells, glia turned out to have more direct roles in promoting normal neuronal and synaptic function.

In a previous work, Botas and his colleagues studied a fruit fly model of HD that expresses the human mutant huntingtin (mHTT) gene in neurons, to understand which of the many gene expression changes that occur in HD are causing disease and which ones are compensatory.

"One class of compensatory changes affected genes involved in synaptic function. Could glia be involved?" Botas said. "To answer this question, we created fruit flies that express mHTT only in glia, only in neurons, or in both cell types."

Comparing changes in gene expression

The researchers began their investigation by comparing the changes in gene expression present in the brains of healthy humans with those in human HD subjects and in HD mouse and fruit fly models. They identified many genes whose expression changed in the same direction across all three species but were particularly intrigued when they discovered that having HD reduces the expression of glial cell genes that contribute to maintaining neuronal connections.

"To investigate whether the reduction of expression of these genes in glia either helped with disease progression or with mitigation, we manipulated each gene either in neurons, glial cells or both cell types in the HD fruit fly model. Then we determined the effect of the gene expression change on the function of the flies' nervous system," Botas said.

They evaluated the flies' nervous system health with a high-throughput automated system that assessed locomotor behavior quantitatively. The system filmed the flies as they naturally climbed up a tube. Healthy flies readily climb, but when their ability to move is compromised, the flies have a hard time climbing. The researchers looked at how the flies move because one of the characteristics of HD is progressive disruption of normal body movements.

Turning down the genes worked

The results revealed that in HD, turning down glial genes involved in synaptic assembly and maintenance is protective.

Fruit flies with the mutant huntingtin gene in their glial cells in which the researchers had deliberately turned down synaptic genes climbed up the tube better than flies in which the synaptic genes were not dialed down.

"Our study reveals that glia affected by HD respond by tuning down synapse genes, which has a protective effect," Botas said. "Some gene expression changes in HD promote disease progression, but other changes in gene expression are protective. Our findings suggest that antagonizing all disease-associated alterations, for example, using drugs to modify gene expression profiles, may oppose the brain's efforts to protect itself from this devastating disease. We propose that researchers studying neurological disorders could deepen their analyses by including glia in their investigations."


References

Doetsch, F., Garcia-Verdugo, J. M. & Alvarez-Buylla, A. Regeneration of a germinal layer in the adult mammalian brain. Proc. Natl Acad. Sci. USA 96, 11619–11624 (1999).

Doetsch, F., Caille, I., Lim, D. A., Garcia-Verdugo, J. M. & Alvarez-Buylla, A. Subventricular zone astrocytes are neural stem cells in the adult mammalian brain. Cell 97, 703–716 (1999). Identified astroglial cells as the source of adult neurogenesis and as adult neural stem cells. This paper has revolutionized our thinking about astroglial cells.

Bedard, A. & Parent, A. Evidence of newly generated neurons in the human olfactory bulb. Brain Res. Dev. Brain Res. 151, 159–168 (2004).

Sanai, N. et al. Unique astrocyte ribbon in adult human brain contains neural stem cells but lacks chain migration. Nature 427, 740–744 (2004).

Alvarez-Buylla, A., Garcia-Verdugo, J. M. & Tramontin, A. D. A unified hypothesis on the lineage of neural stem cells. Nature Rev. Neurosci. 2, 287–293 (2001).

Gabay, L., Lowell, S., Rubin, L. L. & Anderson, D. J. Deregulation of dorsoventral patterning by FGF confers trilineage differentiation capacity on CNS stem cells in vitro. Neuron 40, 485–499 (2003).

Hack, M. A., Sugimori, M., Lundberg, C., Nakafuku, M. & Götz, M. Regionalization and fate specification in neurospheres: the role of Olig2 and Pax6. Mol. Cell. Neurosci. 25, 664–678 (2004).

Garcia, A. D., Doan, N. B., Imura, T., Bush, T. G. & Sofroniew, M. V. GFAP-expressing progenitors are the principal source of constitutive neurogenesis in adult mouse forebrain. Nature Neurosci. 7, 1233–1241 (2004).

Johansson, C. B. et al. Identification of a neural stem cell in the adult mammalian central nervous system. Cell 96, 25–34 (1999).

Capela, A. & Temple, S. LeX/ssea-1 is expressed by adult mouse CNS stem cells, identifying them as nonependymal. Neuron 35, 865–875 (2002).

Seaberg, R. M. & van der Kooy, D. Adult rodent neurogenic regions: the ventricular subependyma contains neural stem cells, but the dentate gyrus contains restricted progenitors. J. Neurosci. 22, 1784–1793 (2002).

Seri, B., Garcia-Verdugo, J. M., McEwen, B. S. & Alvarez-Buylla, A. Astrocytes give rise to new neurons in the adult mammalian hippocampus. J. Neurosci. 21, 7153–7160 (2001).

Niemann, C. & Watt, F. M. Designer skin: lineage commitment in postnatal epidermis. Trends Cell Biol. 12, 185–192 (2002).

Arvidsson, A., Collin, T., Kirik, D., Kokaia, Z. & Lindvall, O. Neuronal replacement from endogenous precursors in the adult brain after stroke. Nature Med. 8, 963–970 (2002).

Lachapelle, F., Avellana-Adalid, V., Nait-Oumesmar, B. & Baron-Van Evercooren, A. Fibroblast growth factor-2 (FGF-2) and platelet-derived growth factor AB (PDGF AB) promote adult SVZ-derived oligodendrogenesis in vivo. Mol. Cell. Neurosci. 20, 390–403 (2002).

Reynolds, B. A. & Weiss, S. Clonal and population analyses demonstrate that an EGF-responsive mammalian embryonic CNS precursor is a stem cell. Dev. Biol. 175, 1–13 (1996).

Rakic, P. A small step for the cell, a giant leap for mankind: a hypothesis of neocortical expansion during evolution. Trends Neurosci. 18, 383–388 (1995).

McConnell, S. K. Constructing the cerebral cortex: neurogenesis and fate determination. Neuron 15, 761–768 (1995).

Gray, G. E., Glover, J. C., Majors, J. & Sanes, J. R. Radial arrangement of clonally related cells in the chicken optic tectum: lineage analysis with a recombinant retrovirus. Proc. Natl Acad. Sci. USA 85, 7356–7360 (1988).

Price, J. & Thurlow, L. Cell lineage in the rat cerebral cortex: a study using retroviral-mediated gene transfer. Development 104, 473–482 (1988).

Luskin, M. B., Pearlman, A. L. & Sanes, J. R. Cell lineage in the cerebral cortex of the mouse studied in-vivo and in-vitro with a recombinant retrovirus. Neuron 1, 635–647 (1988).

Grove, E. A., Williams, B. P., Li, D. -Q., Hajihosseini, M., Friedrich, A. & Price, J. Multiple restricted lineages in the embryonic rat cerebral cortex. Development 117, 553–561 (1993).

Kornack, D. R. & Rakic, P. Radial and horizontal deployment of clonally related cells in the primate neocortex: relationship to distinct mitotic lineages. Neuron 15, 311–321 (1995).

Mione, M. C., Cavanagh, J. F., Harris, B. & Parnavelas, J. G. Cell fate specification and symmetrical/asymmetrical divisions in the developing cerebral cortex. J. Neurosci. 17, 2018–2029 (1997).

Reid, C. B., Tavazoie, S. F. & Walsh, C. A. Clonal dispersion and evidence for asymmetric cell division in ferret cortex. Development 124, 2441–2450 (1997).

Chenn, A. & McConnell, S. K. Cleavage orientation and the asymmetric inheritance of Notch1 immunoreactivity in mammalian neurogenesis. Cell 82, 631–641 (1995). Examined the cell division of neural progenitors live in slice cultures of the developing cerebral cortex. Led to the proposal that the orientation of cell division is correlated with, and predicts, the fate of daugther cells.

Noctor, S. C., Flint, A. C., Weissman, T. A., Dammerman, R. S. & Kriegstein, A. R. Neurons derived from radial glial cells establish radial units in neocortex. Nature 409, 714–720 (2001). Observed the generation of neurons from GFP-labelled radial glial cells using live time-lapse video microscopy in slice cultures from the developing cerebral cortex.

Miyata, T., Kawaguchi, A., Okano, H. & Ogawa, M. Asymmetric inheritance of radial glial fibers by cortical neurons. Neuron 31, 727–741 (2001). Revised the dogma that dividing precursors round up and retract their processes. Time-lapse video microscopy of labelled radial glial cells in cortical slice cultures showed that the radial process is maintained during cell division and is inherited by only one daugther cell.

Noctor, S. C., Martinez-Cerdeno, V., Ivic, L. & Kriegstein, A. R. Cortical neurons arise in symmetric and asymmetric division zones and migrate through specific phases. Nat. Neurosci. 7, 136–144 (2004).

Haubensak, W., Attardo, A., Denk, W. & Huttner, W. B. Neurons arise in the basal neuroepithelium of the early mammalian telencephalon: a major site of neurogenesis. Proc. Natl Acad. Sci. USA 101, 3196–3201 (2004).

Miyata, T. et al. Asymmetric production of surface-dividing and non-surface-dividing cortical progenitor cells. Development 131, 3133–3145 (2004). References 29–31 used time-lapse imaging to describe basal/subventricular zone progenitors, which divide symmetrically to generate two neurons each.

Qian, X., Goderie, S. K., Shen, Q., Stern, J. H. & Temple, S. Intrinsic programs of patterned cell lineages in isolated vertebrate CNS ventricular zone cells. Development 125, 3143–3152 (1998).

Qian, X. et al. Timing of CNS cell generation: a programmed sequence of neuron and glial cell production from isolated murine cortical stem cells. Neuron 28, 69–80 (2000).

Shen, Q., Zhong, W., Jan, Y. N. & Temple, S. Asymmetric Numb distribution is critical for asymmetric cell division of mouse cerebral cortical stem cells and neuroblasts. Development 129, 4843–4853 (2002).

Götz, M., Hartfuss, E. & Malatesta, P. Radial glial cells as neuronal precursors: a new perspective on the correlation of morphology and lineage restriction in the developing cerebral cortex of mice. Brain Res. Bull. 57, 777–788 (2002).

Kriegstein, A. R. & Götz, M. Radial glia diversity: a matter of cell fate. Glia 43, 37–43 (2003).

Fishell, G. & Kriegstein, A. R. Neurons from radial glia: the consequences of asymmetric inheritance. Curr. Opin. Neurobiol. 13, 34–41 (2003).

Huttner, W. B. & Brand, M. Asymmetric division and polarity of neuroepithelial cells. Curr. Opin. Neurobiol. 7, 29–39 (1997). Presents the hypothesis that vertical cleavage planes can result in symmetric and asymmetric divisions of neuroepithelial cells, as such cleavages can either bisect or bypass the apical plasma membrane.

Wodarz, A. & Huttner, W. B. Asymmetric cell division during neurogenesis in Drosophila and vertebrates. Mech. Dev. 120, 1297–1309 (2003).

Weigmann, A., Corbeil, D., Hellwig, A. & Huttner, W. B. Prominin, a novel microvilli-specific polytopic membrane protein of the apical surface of epithelial cells, is targeted to plasmalemmal protrusions of non-epithelial cells. Proc. Natl Acad. Sci. USA 94, 12425–12430 (1997).

Corbeil, D., Röper, K., Fargeas, C. A., Joester, A. & Huttner, W. B. Prominin: a story of cholesterol, plasma membrane protrusions and human pathology. Traffic 2, 82–91 (2001).

Aaku-Saraste, E., Hellwig, A. & Huttner, W. B. Loss of occludin and functional tight junctions, but not ZO-1, during neural tube closure — remodeling of the neuroepithelium prior to neurogenesis. Dev. Biol. 180, 664–679 (1996).

Zhadanov, A. B. et al. Absence of the tight junctional protein AF-6 disrupts epithelial cell–cell junctions and cell polarity during mouse development. Curr. Biol. 9, 880–888 (1999).

Manabe, N. et al. Association of ASIP/mPAR-3 with adherens junctions of mouse neuroepithelial cells. Dev. Dyn. 225, 61–69 (2002).

Aaku-Saraste, E., Oback, B., Hellwig, A. & Huttner, W. B. Neuroepithelial cells downregulate their plasma membrane polarity prior to neural tube closure and neurogenesis. Mech. Dev. 69, 71–81 (1997).

Campbell, K. & Götz, M. Radial glia: multi-purpose cells for vertebrate brain development. Trends Neurosci. 25, 235–238 (2002).

Götz, M. Glial cells generate neurons — master control within CNS regions: developmental perspectives on neural stem cells. Neuroscientist 9, 379–397 (2003).

Williams, B. P. & Price, J. Evidence for multiple precursor cell types in the embryonic rat cerebral cortex. Neuron 14, 1181–1188 (1995).

Malatesta, P., Hartfuss, E. & Götz, M. Isolation of radial glial cells by fluorescent-activated cell sorting reveals a neuronal lineage. Development 127, 5253–5263 (2000). The first direct evidence for a role for radial glial cells as neuronal progenitors.

Malatesta, P. et al. Neuronal or glial progeny: regional differences in radial glia fate. Neuron 37, 751–764 (2003). Showed that there are regional differences in radial glial-cell fate. Radial glial cells from the dorsal telencephalon generate the bulk of neurons in this region, whereas those from the ventral telencephalon generate only a few neurons.

Anthony, T. E., Klein, C., Fishell, G. & Heintz, N. Radial glia serve as neuronal progenitors in all regions of the central nervous system. Neuron 41, 881–890 (2004). This work contradicts the results of reference 50, and indicates that radial glial cells function as neuronal progenitors in all regions of the CNS.

Hartfuss, E., Galli, R., Heins, N. & Gotz, M. Characterization of CNS precursor subtypes and radial glia. Dev. Biol. 229, 15–30 (2001).

Chenn, A., Zhang, Y. A., Chang, B. T. & McConnell, S. K. Intrinsic polarity of mammalian neuroepithelial cells. Mol. Cell. Neurosci. 11, 183–193 (1998).

Halfter, W., Dong, S., Yip, Y. P., Willem, M. & Mayer, U. A critical function of the pial basement membrane in cortical histogenesis. J. Neurosci. 22, 6029–6040 (2002).

Gadisseux, J. F. & Evrard, P. Glial-neuronal relationship in the developing central nervous system. A histochemical-electron microscope study of radial glial cell particulate glycogen in normal and reeler mice and the human fetus. Dev. Neurosci. 7, 12–32 (1985).

Noctor, S. C. et al. Dividing precursor cells of the embryonic cortical ventricular zone have morphological and molecular characteristics of radial glia. J. Neurosci. 22, 3161–3173 (2002).

Williams, B. P. et al. A PDGF-regulated immediate early gene response initiates neuronal differentiation in ventricular zone progenitor cells. Neuron 18, 553–562 (1997).

McCarthy, M., Turnbull, D. H., Walsh, C. A. & Fishell, G. Telencephalic neural progenitors appear to be restricted to regional and glial fates before the onset of neurogenesis. J. Neurosci. 21, 6772–6781 (2001).

Reid, C. B., Liang, I. & Walsh, C. Systematic widespread clonal organization in cerebral cortex. Neuron 15, 299–310 (1995).

Graus-Porta, D. et al. β1-class integrins regulate the development of laminae and folia in the cerebral and cerebellar cortex. Neuron 31, 367–379 (2001).

Turner, D. L. & Cepko, C. A common progenitor for neurons and glia persists in rat retina late in development. Nature 328, 131–136 (1987).

Turner, D. L., Snyder, E. Y. & Cepko, C. L. Lineage-independent determination of cell type in the embryonic mouse retina. Neuron 4, 833–845 (1990).

Leber, S. M. & Sanes, J. R. Migratory paths of neurons and glia in the embryonic chick spinal cord. J. Neurosci. 15, 1236–1248 (1995).

Smart, I. H. M. Proliferative characteristics of the ependymal layer during the early development of the mouse neocortex: a pilot study based on recording the number, location and plane of cleavage of mitotic figures. J. Anat. 116, 67–91 (1973). A classic pioneering study of neuronal progenitor cell division.

Tarabykin, V., Stoykova, A., Usman, N. & Gruss, P. Cortical upper layer neurons derive from the subventricular zone as indicated by Svet1 gene expression. Development 128, 1983–1993 (2001).

Englund, C. et al. Pax6, Tbr2, and Tbr1 are expressed sequentially by radial glia, intermediate progenitor cells, and postmitotic neurons in developing neocortex. J. Neurosci. 25, 247–251 (2005).

Nieto, M. et al. Expression of Cux-1 and Cux-2 in the subventricular zone and upper layers II–IV of the cerebral cortex. J. Comp. Neurol. 479, 168–180 (2004).

Zimmer, C., Tiveron, M. C., Bodmer, R. & Cremer, H. Dynamics of Cux2 expression suggests that an early pool of SVZ precursors is fated to become upper cortical layer neurons. Cereb. Cortex 14, 1408–1420 (2004).

Smart, I. H., Dehay, C., Giroud, P., Berland, M. & Kennedy, H. Unique morphological features of the proliferative zones and postmitotic compartments of the neural epithelium giving rise to striate and extrastriate cortex in the monkey. Cereb. Cortex 12, 37–53 (2002).

Jan, Y. N. & Jan, L. Y. Asymmetric cell division in the Drosophila nervous system. Nature Rev. Neurosci. 2, 772–779 (2001).

Knoblich, J. A. Asymmetric cell division during animal development. Nature Rev. Mol. Cell Biol. 2, 11–20 (2001).

Landrieu, P. & Goffinet, A. Mitotic spindle fiber orientation in relation to cell migration in the neo-cortex of normal and reeler mouse. Neurosci. Lett. 13, 69–72 (1979).

Kosodo, Y. et al. Asymmetric distribution of the apical plasma membrane during neurogenic divisions of mammalian neuroepithelial cells. EMBO J. 23, 2314–2324 (2004). This study confirmed the hypothesis proposed in reference 38 that vertical cleavage planes can result in symmetric and asymmetric divisions of neuroepithelial cells.

Iacopetti, P. et al. Expression of the antiproliferative gene TIS21 at the onset of neurogenesis identifies single neuroepithelial cells that switch from proliferative to neuron-generating division. Proc. Natl Acad. Sci. USA 96, 4639–4644 (1999). This paper describes the first pan-neurogenic marker, Tis21 , which is expressed in progenitors that undergo neurogenic divisions, but not in progenitors that undergo proliferative divisions.

Heins, N. et al. Emx2 promotes symmetric cell divisions and a multipotential fate in precursors from the cerebral cortex. Mol. Cell. Neurosci. 18, 485–502 (2001).

Heins, N. et al. Glial cells generate neurons: the role of the transcription factor Pax6. Nature Neurosci. 5, 308–315 (2002). This work shows that PAX6 is important for the neurogenesis of radial glial cells in the developing cerebral cortex, and is also sufficient to instruct the neurogenesis of postnatal astrocytes in vitro.

Gönczy, P., Grill, S., Stelzer, E. H., Kirkham, M. & Hyman, A. A. Spindle positioning during the asymmetric first cell division of Caenorhabditis elegans embryos. Novartis Found. Symp. 237, 164–175 (2001).

Haydar, T. F., Ang, E. Jr . & Rakic, P. Mitotic spindle rotation and mode of cell division in the developing telencephalon. Proc. Natl Acad. Sci. USA 100, 2890–2895 (2003).

Reinsch, S. & Karsenti, E. Orientation of spindle axis and distribution of plasma membrane proteins during cell division in polarized MDCKII cells. J. Cell Biol. 126, 1509–1526 (1994).

Bond, J. et al. ASPM is a major determinant of cerebral cortical size. Nature Genet. 32, 316–320 (2002).

Kouprina, N. et al. Accelerated evolution of the ASPM gene controlling brain size begins prior to human brain expansion. PLoS Biol. 2, 653–663 (2004).

Bond, J. et al. Protein-truncating mutations in ASPM cause variable reduction in brain size. Am. J. Hum. Genet. 73, 1170–1177 (2003).

Burgess, R. W., Deitcher, D. L. & Schwarz, T. L. The synaptic protein syntaxin1 is required for cellularization of Drosophila embryos. J. Cell Biol. 138, 861–875 (1997).

Nacry, P., Mayer, U. & Jurgens, G. Genetic dissection of cytokinesis. Plant Mol. Biol. 43, 719–733 (2000).

Glotzer, M. Animal cell cytokinesis. Annu. Rev. Cell Dev. Biol. 17, 351–386 (2001).

Low, S. H. et al. Syntaxin 2 and endobrevin are required for the terminal step of cytokinesis in mammalian cells. Dev. Cell 4, 753–759 (2003).

Mostov, K. E., Verges, M. & Altschuler, Y. Membrane traffic in polarized epithelial cells. Curr. Opin. Cell Biol. 12, 483–490 (2000).

Low, S. H. et al. Retinal pigment epithelial cells exhibit unique expression and localization of plasma membrane syntaxins which may contribute to their trafficking phenotype. J. Cell Sci. 115, 4545–4553 (2002).

Rothman, J. E. Mechanisms of intracellular protein transport. Nature 372, 55–63 (1994).

Jahn, R. & Südhof, T. C. Membrane fusion and exocytosis. Annu. Rev. Biochem. 68, 863–911 (1999).

Chae, T. H., Kim, S., Marz, K. E., Hanson, P. I. & Walsh, C. A. The HYH mutation uncovers roles for α-SNAP in apical protein localization and control of neural cell fate. Nature Genet. 36, 264–270 (2004).

Sheen, V. L. et al. Mutations in ARFGEF2 implicate vesicle trafficking in neural progenitor proliferation and migration in the human cerebral cortex. Nature Genet. 36, 69–76 (2004).

Saito, K. et al. Morphological asymmetry in dividing retinal progenitor cells. Dev. Growth Differ. 45, 219–229 (2003).

Roegiers, F. & Jan, Y. N. Asymmetric cell division. Curr. Opin. Cell Biol. 16, 195–205 (2004).

Schweisguth, F. Regulation of Notch signaling activity. Curr. Biol. 14, R129–R138 (2004).

Zhong, W. Diversifying neural cells through order of birth and asymmetry of division. Neuron 37, 11–14 (2003).

Kerjaschki, D., Noronha-Blob, L., Sacktor, B. & Farquhar, M. G. Microdomains of distinctive glycoprotein composition in the kidney proximal tubule brush border. J. Cell Biol. 98, 1505–1513 (1984).

Herz, J. & Bock, H. H. Lipoprotein receptors in the nervous system. Annu. Rev. Biochem. 71, 405–434 (2002).

May, P. & Herz, J. LDL receptor-related proteins in neurodevelopment. Traffic 4, 291–301 (2003).

Machold, R. et al. Sonic hedgehog is required for progenitor cell maintenance in telencephalic stem cell niches. Neuron 39, 937–950 (2003).

Fargeas, C. A., Corbeil, D. & Huttner, W. B. AC133 antigen, CD133, prominin-1, prominin-2, etc. : prominin family gene products in need of a rational nomenclature. Stem Cells 21, 506–508 (2003).

Röper, K., Corbeil, D. & Huttner, W. B. Retention of prominin in microvilli reveals distinct cholesterol-based lipid microdomains in the apical plasma membrane. Nature Cell Biol. 2, 582–592 (2000).

Takekuni, K. et al. Direct binding of cell polarity protein PAR-3 to cell–cell adhesion molecule nectin at neuroepithelial cells of developing mouse. J. Biol. Chem. 278, 5497–500 (2003).

Lin, D. et al. A mammalian PAR-3–PAR-6 complex implicated in Cdc42/Rac1 and aPKC signalling and cell polarity. Nature Cell Biol. 2, 540–547 (2000).

Ohno, S. Intercellular junctions and cellular polarity: the PAR–aPKC complex, a conserved core cassette playing fundamental roles in cell polarity. Curr. Opin. Cell Biol. 13, 641–648 (2001).

Chenn, A. & Walsh, C. A. Increased neuronal production, enlarged forebrains and cytoarchitectural distortions in β-catenin overexpressing transgenic mice. Cereb. Cortex 13, 599–606 (2003).

Chenn, A. & Walsh, C. A. Regulation of cerebral cortical size by control of cell cycle exit in neural precursors. Science 297, 365–369 (2002).

Zechner, D. et al. β-Catenin signals regulate cell growth and the balance between progenitor cell expansion and differentiation in the nervous system. Dev. Biol. 258, 406–418 (2003).

Machon, O., van den Bout, C. J., Backman, M., Kemler, R. & Krauss, S. Role of β-catenin in the developing cortical and hippocampal neuroepithelium. Neuroscience 122, 129–143 (2003).

Sauer, F. C. Mitosis in the neural tube. J. Comp. Neurol. 62, 377–405 (1935).

Takahashi, T., Nowakowski, R. S. & Caviness, V. S. Cell cycle parameters and patterns of nuclear movement in the neocortical proliferative zone of the fetal mouse. J. Neurosci. 13, 820–833 (1993).

Frade, J. M. Interkinetic nuclear movement in the vertebrate neuroepithelium: encounters with an old acquaintance. Prog. Brain Res. 136, 67–71 (2002).

Messier, P. -E. & Auclair, C. Inhibition of nuclear migration in the absence of microtubules in the chick embryo. J. Embryol. Exp. Morph. 30, 661–671 (1973).

Messier, P. E. Microtubules, interkinetic nuclear migration and neurulation. Experientia 34, 289–296 (1978).

Reinsch, S. & Gönczy, P. Mechanisms of nuclear positioning. J. Cell Sci. 111, 2283–2295 (1998).

Morris, N. R. Nuclear positioning: the means is at the ends. Curr. Opin. Cell Biol. 15, 54–59 (2003).

Faulkner, N. E. et al. A role for the lissencephaly gene lis1 in mitosis and cytoplasmic dynein function. Nature Cell Biol. 2, 784–791 (2000).

Sapir, T., Elbaum, M. & Reiner, O. Reduction of microtubule catastrophe events by LIS1, platelet-activating factor acetylhydrolase subunit. EMBO J. 16, 6977–6984 (1997).

Olson, E. C. & Walsh, C. A. Smooth, rough and upside-down neocortical development. Curr. Opin. Genet. Dev. 12, 320–327 (2002).

Gambello, M. J. et al. Multiple dose-dependent effects of Lis1 on cerebral cortical development. J. Neurosci. 23, 1719–1729 (2003).

MacLean-Fletcher, S. & Pollard, T. D. Mechanism of action of cytochalasin B on actin. Cell 20, 329–341 (1980).

Karfunkel, P. The activity of microtubules and microfilaments in neurulation in the chick. J. Exp. Zool. 181, 289–301 (1972).

Messier, P. -E. & Auclair, C. Effect of cytochalasin B on interkinetic nuclear migration in the chick embryo. Dev. Biol. 36, 218–223 (1974).

Tullio, A. N. et al. Structural abnormalities develop in the brain after ablation of the gene encoding nonmuscle myosin II-B heavy chain. J. Comp. Neurol. 433, 62–74 (2001).

Götz, M., Stoykova, A. & Gruss, P. Pax6 controls radial glia differentiation in the cerebral cortex. Neuron 21, 1031–1044 (1998).

Estivill-Torrus, G., Pearson, H., van Heyningen, V., Price, D. J. & Rashbass, P. Pax6 is required to regulate the cell cycle and the rate of progression from symmetrical to asymmetrical division in mammalian cortical progenitors. Development 129, 455–466 (2002).

Murciano, A., Zamora, J., Lopez-Sanchez, J. & Frade, J. M. Interkinetic nuclear movement may provide spatial clues to the regulation of neurogenesis. Mol. Cell. Neurosci. 21, 285–300 (2002).

Calegari, F. & Huttner, W. B. An inhibition of cyclin-dependent kinases that lengthens, but does not arrest, neuroepithelial cell cycle induces premature neurogenesis. J. Cell Sci. 116, 4947–4955 (2003). This study formulates the cell-cycle length hypothesis, which is supported by the finding that lengthening the cell cycle of neuroepithelial cells can be sufficient to switch neuroepithelial cells from proliferative to neurogenic divisions.

Takahashi, T., Nowakowski, R. S. & Caviness, V. S. The cell cycle of the pseudostratified ventricular epithelium of the embryonic murine cerebral wall. J. Neurosci. 15, 6046–6057 (1995). A seminal study showing that the cell cycle of ventricular zone cells lengthens concomitant with the onset and progression of neurogenesis.

Durand, B. & Raff, M. A cell-intrinsic timer that operates during oligodendrocyte development. Bioessays 22, 64–71 (2000).

Ohnuma, S., Philpott, A. & Harris, W. A. Cell cycle and cell fate in the nervous system. Curr. Opin. Neurobiol. 11, 66–73 (2001).

Cremisi, F., Philpott, A. & Ohnuma, S. Cell cycle and cell fate interactions in neural development. Curr. Opin. Neurobiol. 13, 26–33 (2003).

Bally-Cuif, L. & Hammerschmidt, M. Induction and patterning of neuronal development, and its connection to cell cycle control. Curr. Opin. Neurobiol. 13, 16–25 (2003).

Ohnuma, S. & Harris, W. A. Neurogenesis and the cell cycle. Neuron 40, 199–208 (2003).

Matsuda, S., Rouault, J., Magaud, J. & Berthet, C. In search of a function for the TIS21/PC3/BTG1/TOB family. FEBS Lett. 497, 67–72 (2001).

Tirone, F. The gene PC3 TIS21/BTG2 , prototype member of the PC3/BTG/TOB family: regulator in control of cell growth, differentiation, and DNA repair? J. Cell Physiol. 187, 155–165 (2001).

Malatesta, P. et al. PC3 overexpression affects the pattern of cell division of rat cortical precursors. Mech. Dev. 90, 17–28 (2000).

Canzoniere, D. et al. Dual control of neurogenesis by PC3 through cell cycle inhibition and induction of Math1. J. Neurosci. 24, 3355–3369 (2004).

Lukaszewicz, A., Savatier, P., Cortay, V., Kennedy, H. & Dehay, C. Contrasting effects of basic fibroblast growth factor and neurotrophin 3 on cell cycle kinetics of mouse cortical stem cells. J. Neurosci. 22, 6610–6622 (2002).

Takahashi, T., Nowakowski, R. S. & Caviness, V. S. The leaving or Q fraction of the murine cerebral proliferative epithelium: a general model of neocortical neuronogenesis. J. Neurosci. 16, 6183–6196 (1996).

Hatakeyama, J. et al. Hes genes regulate size, shape and histogenesis of the nervous system by control of the timing of neural stem cell differentiation. Development 131, 5539–5550 (2004).

Klezovitch, O., Fernandez, T. E., Tapscott, S. J. & Vasioukhin, V. Loss of cell polarity causes severe brain dysplasia in Lgl1 knockout mice. Genes Dev. 18, 559–571 (2004).

Doetsch, F., Petreanu, L., Caille, I., Garcia-Verdugo, J. M. & Alvarez-Buylla, A. EGF converts transit-amplifying neurogenic precursors in the adult brain into multipotent stem cells. Neuron 36, 1021–1034 (2002).

Spoelgen, R. et al. LRP2/megalin is required for patterning of the ventral telencephalon. Development 132, 405–414 (2005).

Calegari, F., Haubensak, W., Haffner, C. & Huttner, W. B. Selective lengthening of the cell cycle in the neurogenic subpopulation of neural progenitor cells during mouse brain development. J. Neurosci. 25, 6533–6538 (2005).


New glial cells discovered in the brain: Implications for brain repair

Neurons, nerve cells in the brain, are central players in brain function. However, a key role for glia, long considered support cells, is emerging. A research group at the University of Basel has now discovered two new types of glial cells in the brain, by unleashing adult stem cells from their quiescent state. These new types of glia may play an important role in brain plasticity and repair.

The brain is malleable well into adulthood. Brain plasticity is not only due to the formation of new nerve connections. Stem cells present in the adult brain also generate new nerve cells. For more than a hundred years, scientists have concentrated on investigating different types of nerve cells.

In the brain, however, another class of cells, called glia, are also essential for brain function. However, the importance of glial cells has been underestimated for decades. How many types of glia there are, how they develop and what roles they play are all still largely unexplored.

Stem cells - unleashed from quiescence

The research group of Prof. Fiona Doetsch at the Biozentrum of the University of Basel is investigating stem cells in the ventricular-subventricular zone in the adult mouse brain. In this region, many of the stem cells are in a quiescent state, sensing signals in the environment that stimulate them to awaken and transform into new nerve cells.

In their study in the journal Science, Doetsch's team identified a molecular signal that awakened the stem cells from their quiescent state, allowing them to uncover multiple domains that give rise to glial cells in this stem cell reservoir.

Stem cells - birthplace of glial cells

"We found an activation switch for quiescent stem cells," Doetsch explains. "It is a receptor that maintains the stem cells in their resting state. We were able to turn off this switch and thus activate the stem cells," Doetsch says. In addition, the researchers were able to visualize the development of the stem cells into different glial cells in specific areas of the stem cell niche.

"Some of the stem cells did not develop into neurons, but into two different novel types of glial cells," Doetsch reports. This brain region studied is therefore a birthplace for different types of glial cells as well as its role as a breeding ground for neurons.

"What was very unexpected was that one glial cell type was found attached to the surface of the wall of the brain ventricle, rather than in the brain tissue." These cells are continuously bathed by cerebrospinal fluid and interact with axons from other brain areas, and therefore are poised to sense and integrate multiple long-range signals.

Glial cells - active in health and disease

The research team also found that both glial cell types were activated in a model of demyelination. These new glial cell types may therefore be a source of cells for repair in neurodegenerative diseases, such as multiple sclerosis or after injury.

As a next step, Doetsch would like to specifically trace these new glial cell types and to investigate their roles in normal brain function and how they respond in different physiological contexts. This will provide important clues to understanding brain plasticity and how the renewal and repair of neural tissue occurs.

Disclaimer: AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert system.


Neurogenesis

At one time, scientists believed that people were born with all the neurons they would ever have. Research performed during the last few decades indicates that neurogenesis, the birth of new neurons, continues into adulthood. Neurogenesis was first discovered in songbirds that produce new neurons while learning songs. For mammals, new neurons also play an important role in learning: about 1000 new neurons develop in the hippocampus (a brain structure involved in learning and memory) each day. While most of the new neurons will die, researchers found that an increase in the number of surviving new neurons in the hippocampus correlated with how well rats learned a new task. Interestingly, both exercise and some antidepressant medications also promote neurogenesis in the hippocampus. Stress has the opposite effect. While neurogenesis is quite limited compared to regeneration in other tissues, research in this area may lead to new treatments for disorders such as Alzheimer’s, stroke, and epilepsy.

How do scientists identify new neurons? A researcher can inject a compound called bromodeoxyuridine (BrdU) into the brain of an animal. While all cells will be exposed to BrdU, BrdU will only be incorporated into the DNA of newly generated cells that are in S phase. A technique called immunohistochemistry can be used to attach a fluorescent label to the incorporated BrdU, and a researcher can use fluorescent microscopy to visualize the presence of BrdU, and thus new neurons, in brain tissue. Figure 16.6 is a micrograph which shows fluorescently labeled neurons in the hippocampus of a rat.

Figure 16.6. This micrograph shows fluorescently labeled new neurons in a rat hippocampus. Cells that are actively dividing have bromodoxyuridine (BrdU) incorporated into their DNA and are labeled in red. Cells that express glial fibrillary acidic protein (GFAP) are labeled in green. Astrocytes, but not neurons, express GFAP. Thus, cells that are labeled both red and green are actively dividing astrocytes, whereas cells labeled red only are actively dividing neurons. (credit: modification of work by Dr. Maryam Faiz, et. al., University of Barcelona scale-bar data from Matt Russell)


CG11426 gene product negatively regulates glial population size in the drosophila eye imaginal disc

Sang-Hak Jeon, Ph.D., Department of Science Education/Biology Education, Seoul National University, Seoul, Korea.

Department of Biology Education, Seoul National University, Seoul, Republic of Korea

Department of Biology Education, Seoul National University, Seoul, Republic of Korea

Department of Biochemistry & Cellular and Molecular Biology, and Neuronet Research Center, University of Tennessee, Knoxville, 37996 USA

Department of Biochemistry & Cellular and Molecular Biology, and Neuronet Research Center, University of Tennessee, Knoxville, 37996 USA

Department of Biology Education, Seoul National University, Seoul, Republic of Korea

Korea Basic Science Institute, Seoul Center, 02841 Korea

Department of Biology Education, Seoul National University, Seoul, Republic of Korea

Sang-Hak Jeon, Ph.D., Department of Science Education/Biology Education, Seoul National University, Seoul, Korea.

This article has been accepted for publication and undergone full peer review but has not been through the copyediting, typesetting, pagination and proofreading process, which may lead to differences between this version and the Version of Record. Please cite this article as https://doi.org/10.1002/dneu.22838

ABSTRACT

Glial cells play essential roles in the nervous system. Although glial populations are tightly regulated, the mechanisms regulating the population size remain poorly understood. Since Drosophila glial cells are similar to the human counterparts in their functions and shapes, rendering them an excellent model system to understand the human glia biology. Lipid phosphate phosphatases (LPP) are important for regulating bioactive lipids. In Drosophila, there are three known LPP-encoding genes wunen, wunen-2 and lazaro. The wunens are important for the germ cell migration and survival, and septate junction formation during tracheal development. Lazaro is involved in phototransduction. In the present study, we characterized a novel Drosophila LPP-encoding gene, CG11426. Suppression of CG11426 increased glial cell number in the eye imaginal disc during larval development, while ectopic CG11426 expression decreased it. Both types of mutation also caused defects in axon projection to the optic lobe in larval eye–brain complexes. Moreover, CG11426 promoted apoptosis via inhibiting ERK signaling in the eye imaginal disc. Taken together, these findings demonstrated that CG11426 gene product negatively regulates ERK signaling to promote apoptosis for proper maintenance of glial population in the developing eye disc.

This article is protected by copyright. All rights reserved

Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.

Accepted, unedited articles published online and citable. The final edited and typeset version of record will appear in the future.


SOFC-XVII

The International Symposium on Solid Oxide Fuel Cells has been the preeminent meeting on SOFC science, technology, and applications for over 30 years, consistently attracting hundreds of the leaders in the field. Join us for five days of learning, networking, and collaborating.

To Exhibit | June 11, 2021
To Sponsor | June 11, 2021

ECST Submission Site Open: March 15 – May 14, 2021

To Submit Presentation Files: July 9, 2021

"Open data is the only way to move the world forward, learning from give and take to find new ways to connect the dots and have new insights, that is what electrochemistry has done already for hundreds of years."

-Koen Kas, 235th ECS Meeting plenary speaker

Footer Menu

Footer Menu

Footer Menu

We are using cookies to give you the best experience on our website.

This website uses cookies so that we can provide you with the best user experience possible. Cookie information is stored in your browser and performs functions such as recognising you when you return to our website and helping our team to understand which sections of the website you find most interesting and useful.


Glial cells

Glial cells support neurons and maintain their environment. Glial cells of the (a) central nervous system include oligodendrocytes, astrocytes, ependymal cells, and microglial cells. Oligodendrocytes form the myelin sheath around axons.

Glial cells
Glial cells (named from the Greek for "glue") are non-neuronal cells that provide support and nutrition, maintain homeostasis, form myelin, and participate in signal transmission in the nervous system.

glial cells Nonconducting cells that serve as support cells in the nervous system and help to protect neurons.
glomerulus A tangle of capillaries that makes up part of the nephron the site of ?ltration.

Supportive cells that are closely associated with neurons.
global environmental citizenship A shift in our attention from pollution in a specific place to a concern about the life-support systems of the whole planet.

Non-neuronal cells found in the brain and other parts of the nervous system. Their roles include supporting neurons and forming the myelin sheath. Glucose .

Nonexcitable supportive cells in the nervous system also called neuroglial cells. Include astrocytes and oligodendrocytes in the vertebrate central nervous system and Schwann cells in the peripheral nervous system.
glucagon .

(astrocytes, microgliacytes, ependymal cells and oligodendrocytes) are the cells that support, feed and insulate (electrically) the neurons.

constitute the most abundant class of cells in the brain and can generally be subdivided into astrocytes, oligodendrocytes and microglia based on morphology and function.

- supporting cells of the nervous system, including oligodendrocytes and astrocytes in the vertebrate central nervous system and Schwann cells in the peripheralnervous system .

, also called astrocytes, are star-shaped cells found in the brain and spinal cord. They provide nutrients to neurons, maintain ion balance, and remove unneeded excess neurotransmitters from the synaptic cleft.
Ependymal cells are also found in the CNS. There are two types of ependymal cells.

are responsible for immunohomeostatic response to CNS, and have different functions (Kettenmann et al., 2011). The most essential function of Microglia is phagocytosis, known for engulfment of various cells via actin-myosin contractile system (Stuart and Ezekowitz, 2005).

(embryonic neural stem cells) that give rise to excitatory neurons in the fetal brain through the process of neurogenesis.[10][11][12]
Hematopoietic stem cells (adult stem cells) from the bone marrow that give rise to red blood cells, white blood cells, and platelets .

, the V max =53 μM/hr and the K m =4.2 μM for V HNMTg.
MAT
We took the K m =24 μM of the monoamine transporter from [23] and we include a linear backleak term from the vesicular compartment to the cytosol as indicated in [24] for dopamine.

The nervous system uses two different kinds of cells one is called

and those are the ones that help support and maintain the other cells and those other cells are the neurons the ones that are considered they' .

There are stem cells in neural tissue that give rise to neurons and astro

and things like that. And muscle has stem cells. And there are many different kinds of stem cells that have been identified in adults.

In addition, there are perhaps nine times as many

, whose exact roles are unclear, but which help to support and maintain neurons. Most neurons are present shortly after birth, and as the brain continues to grow, the number and complexity of neuronal connections increases.

In vertebrates generally, the axons of many neurons are sheathed in myelin, which is formed by either of two types of

: Schwann cells ensheathing peripheral neurons and oligodendrocytes insulating those of the central nervous system.

The small gaps in the myelin sheath between successive

along the axon of a neuron also, the site of high concentration of voltage-gated ion channels.
nomograph
A graph that allows a third variable to be measured when the values of two related variables are known.

nervous tissue Tissue composed of neurons and

. Nervous tissue is one the four classes to which tissue has traditionally been assigned, the other three being muscle, epithelial tissue, and connective tissue.
Online Biology Dictionary (NEUR-) .

lining the ventricles of the brain and the central canal of the spinal cord. (Google Dictionary) 3. Thin epithelial membrane lining the ventricles of the brain and the spinal cord canal.

A regulatory system of the body that consists of neurons and neuroglial cells. The nervous system is divided into two parts, the central nervous system (CNS) and the peripheral nervous system (PNS).

The results showed that autism shares quite a bit in common with schizophrenia and bipolar disorder, but it also diverges in several key places. Activity in genes specifically related to micro

were unique to autistic brains, .

FIG. 667- Section of central canal of medulla spinalis, showing ependymal and neuroglial cells. (v. Lenhossek.) (See enlarged image) .

the brain are made up of about 100 billion neurons, as well as trillions of support cells called glia. Neurons may be the more important cells in the brain that relay messages about what you&aposre thinking, feeling, or doing. But they couldn&apost do it without a little help from their friends, the

include peripherin, neurofilaments, and glial fibrillary acidic protein (GFAP).


Watch the video: Part 4 - Glial Cells (August 2022).