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'''Astrocytes''' ( | '''Astrocytes''' (or '''astroglia''') are star-shaped [[neuroglia|glial]] [[cell (biology)|cells]] in the [[brain]] and [[spinal cord]]. They have many functions, including biochemical support of [[epithelial cell]]s that form the [[blood-brain barrier]], the provision of nutrients to the nervous tissue, and thay have a major role in the repair and scarring process in the brain. They also intercommunicate with neurones, and have an important role in the uptake and degradation of neurotransmitters released by neurons into the extracellular space. | ||
==Description== | ==Description== | ||
Astrocytes are a sub-type of the [[glial cells]] | Astrocytes are a sub-type of the [[glial cells]]. Their primary processes are star-shaped, and numerous fine processes largely fill the space between the "star beams" to create a ''spongiform'' shape. Fine distal processes of the astrocyte envelop, or "ensheath" neurons and their [[axons]]. Proximity and interaction between synaptic elements and astrocytic processes gave rise to a concept of "tripartite synapse"<ref>{{cite journal |author=Araque A ''et al.'' |title=Tripartite synapses: glia, the unacknowledged partner |journal=Trends Neurosci. |volume=22 |pages=208–15 |year=1999 |pmid=10322493 }}</ref>. The degree of synapse ensheathing varies between brain areas and between individual synapses, and it can also change in an activity-dependent manner, allowing for structural plasticity of tripartite synapse. Astrocytes express many different receptors for [[peptides]] and other signalling molecules that are released by neurons, and these signals regulate their shape and function. | ||
Classically, astrocytes are identified histologically by their expression of the intermediate filament [[glial fibrillary acidic protein]] (GFAP), although the level of GFAP expression varies widely between astrocytes. Two forms of astrocytes exist in the CNS, ''fibrous'' and ''protoplasmic''. Fibrous astrocytes are usually located within white matter, have relatively few organelles, and have long, unbranched processes. This type often has "vascular feet", also called endfeet, that connect the astrocyte to the outside of capillary wall. ''Protoplasmic astrocytes'', found in grey matter, have more organelles, and short,highly branched processes. When in proximity to the [[pia mater]], astrocytes send out their processes to form the pia-glial membrane. | |||
Formerly, astrocytes were looked upon as ''gap fillers'' in the CNS, playing essentially a supportive, structural role. However, astrocytic networks are now thought to play a number of active roles in the brain, including the secretion and uptake of neurotransmitters, "siphoning" K<sup>+</sup> ions away from synapses, regulation of [[synaptogenesis]], modulation of [[synaptic transmission]], short- and long-term [[synaptic plasticity]], [[neuro-vascular coupling]], maintenance of the [[blood-brain barrier]] and more. | |||
==Functions== | ==Functions== | ||
* '''Structural''': involved in the physical structuring of the brain. | * '''Structural''': involved in the physical structuring of the brain. | ||
* '''Metabolic support''': | * '''Metabolic support''': providing neurons with nutrients such as [[glucose]]. | ||
* '''[[Blood-brain barrier]]''': the astrocyte end-feet encircling [[endothelial cell]]s were thought to aid in the maintenance of the blood-brain barrier, but recent research indicates that | * '''[[Blood-brain barrier]]''': the astrocyte end-feet encircling [[endothelial cell]]s were thought to aid in the maintenance of the blood-brain barrier, but recent research indicates that the [[tight junctions]] and [[basal lamina]] of the cerebral endothelial cells that play the most substantial role in maintaining the barrier. | ||
* '''Transmitter reuptake and release''': astrocytes express plasma membrane transporters such as [[glutamate transporter]]s for several neurotransmitters, including [[glutamate]], ATP and [[GABA]]. More recently, astrocytes | * '''Transmitter reuptake and release''': astrocytes express plasma membrane transporters such as [[glutamate transporter]]s for several neurotransmitters, including [[glutamate]], ATP and [[GABA]]. More recently, astrocytes have been shown shown to release glutamate or [[adenosine triphosphate|ATP]] in a vesicular, Ca<sup>2+</sup>-dependent manner.<ref>{{cite journal | author = Santello M, Volterra A | title = Synaptic modulation by astrocytes via Ca(2+)-dependent glutamate release. | journal = Neuroscience | volume = Mar 22 | [Epub ahead of print] | year = 2008 | pmid = 18455880 }} </ref><ref>{{cite journal | author = Pryazhnikov E, Khiroug L. | title = Synaptic Sub-micromolar increase in [Ca(2+)](i) triggers delayed exocytosis of ATP in cultured astrocytes. | journal = Glia | volume = 56:38-49. | year = 2008 | pmid = 17910050 }} </ref> | ||
* '''Regulation of ion concentration in the extracellular space''': astrocytes express [[potassium channels]] at a high density. When neurons are active, they release potassium, increasing the local extracellular concentration. Because astrocytes are highly permeable to potassium, they rapidly clear the excess accumulation in the extracellular space. If this function is interfered with, the extracellular concentration of potassium will rise, leading to neuronal depolarization by the [[Goldman equation]]. Abnormal accumulation of extracellular potassium | * '''Regulation of ion concentration in the extracellular space''': astrocytes express [[potassium channels]] at a high density. When neurons are active, they release potassium, increasing the local extracellular concentration. Because astrocytes are highly permeable to potassium, they rapidly clear the excess accumulation in the extracellular space. If this function is interfered with, the extracellular concentration of potassium will rise, leading to neuronal depolarization by the [[Goldman equation]]. Abnormal accumulation of extracellular potassium can result in epileptic neuronal activity. | ||
* '''Modulation of synaptic transmission''': in the [[supraoptic nucleus]] of the [[hypothalamus]], rapid changes in | * '''Modulation of synaptic transmission''': in the [[supraoptic nucleus]] of the [[hypothalamus]], rapid changes in the morphology of astrocytes occur in a variety of different physiological states, including [[lactation]]. These changes been shown to affect heterosynaptic transmission between neurons.<ref>{{cite journal | author = Piet R ''et al.''| title = Physiological contribution of the astrocytic environment of neurons to intersynaptic crosstalk | journal = Proc Natl Acad Sci U S A | volume = 101 | pages = 2151–5 | year = 2004 | pmid = 14766975 }}</ref> | ||
* '''Vasomodulation''': astrocytes may serve as intermediaries in neuronal regulation of blood flow.<ref>{{cite journal | author = Parri R, Crunelli V | title = An astrocyte bridge from synapse to blood flow | journal = Nat Neurosci | volume = 6 | * '''Vasomodulation''': astrocytes may serve as intermediaries in neuronal regulation of blood flow.<ref>{{cite journal | author = Parri R, Crunelli V | title = An astrocyte bridge from synapse to blood flow | journal = Nat Neurosci | volume = 6 | pages = 5–6 | year = 2003 | pmid = 12494240 }}</ref> | ||
* '''Promotion of the myelinating activity of [[oligodendrocyte]]s''': electrical activity in neurons causes them to release ATP, which serves as an important stimulus for myelin to form. Surprisingly, | * '''Promotion of the myelinating activity of [[oligodendrocyte]]s''': electrical activity in neurons causes them to release ATP, which serves as an important stimulus for myelin to form. Surprisingly, ATP does not act directly on oligodendrocytes; instead it causes astrocytes to secrete the cytokine [[leukemia inhibitory factor]], a regulatory protein that promotes the myelinating activity of oligodendrocytes. <ref>{{cite journal | author = Ishibashi T ''et al.'' | title = Astrocytes promote myelination in response to electrical impulses | journal = Neuron | volume = 49 | pages = 823–32 | year = 2006 | pmid = 16543131 }}</ref> | ||
* '''Nervous system repair''': upon injury to nerve cells | * '''Nervous system repair''': upon injury to nerve cells , astrocytes become phagocytic to ingest the injured nerve cells. The astrocytes then fill up the space to form a [[glial scar]], repairing the area and replacing the CNS cells that cannot regenerate. | ||
Astrocytes are important in regulating neural [[stem cell]]s. The human brain contains numerous neural [[stem cell]]s, which are kept in a dormant state by chemical signals (ephrin-A2 and ephrin-A3) from the astrocytes. Astrocytes can activate the stem cells to transform into working neurons by dampening the release of [[ephrin-A2]] and [[ephrin-A3]]. | |||
==Calcium waves== | ==Calcium waves== | ||
Astrocytes are linked by [[gap junction]]s, creating an electrically coupled [[syncytium]].<ref>{{cite journal | author = Bennett M | Astrocytes are linked by [[gap junction]]s, creating an electrically coupled [[syncytium]].<ref>{{cite journal | author = Bennett M ''et al.''| title = New roles for astrocytes: gap junction hemichannels have something to communicate | journal = Trends Neurosci | volume = 26 | pages = 610–7 | year = 2003 | pmid = 14585601 }}</ref> Waves of intracellular calcium can propagate outwards through this syncytium. Mechanisms of calcium wave propagation include diffusion of [[IP3]] through gap junctions and extracellular ATP signalling.<ref>Newman, J (2001) ''Neuroscience'' 21:2215-23</ref> Calcium elevations are the primary known axis of activation in astrocytes, and are necessary and sufficient for some types of astrocytic glutamate release.<ref>{{cite journal | author = Parpura V, Haydon P | title = Physiological astrocytic calcium levels stimulate glutamate release to modulate adjacent neurons | journal = Proc Natl Acad Sci U S A | volume = 97 | pages = 8629–34 | year = 2000 | pmid = 10900020 }}</ref> | ||
==Classification== | ==Classification== | ||
There are several | There are several ways to classify astrocytes: | ||
'''(1) By lineage and antigenic phenotype''' | '''(1) By lineage and antigenic phenotype''' | ||
from the classic studies of Raff ''et al.'' on rat optic nerves. | |||
* Type 1: Antigenically Ran2<sup>+</sup>, GFAP<sup>+</sup>, FGFR3<sup>+</sup>, A2B5<sup>-</sup> thus resembling the "type 1 astrocyte" of the postnatal day 7 rat optic nerve. These can arise from the tripotential glial restricted precursor cells (GRP), but not from the bipotential O2A/OPC (oligodendrocyte, type 2 astrocyte precursor, also called ''[[Oligodendrocyte precursor cell|Oligodendrocye progenitor cell]]'') cells. | * Type 1: Antigenically Ran2<sup>+</sup>, GFAP<sup>+</sup>, FGFR3<sup>+</sup>, A2B5<sup>-</sup> thus resembling the "type 1 astrocyte" of the postnatal day 7 rat optic nerve. These can arise from the tripotential glial restricted precursor cells (GRP), but not from the bipotential O2A/OPC (oligodendrocyte, type 2 astrocyte precursor, also called ''[[Oligodendrocyte precursor cell|Oligodendrocye progenitor cell]]'') cells. | ||
* Type 2: Antigenically A2B5<sup>+</sup>, GFAP<sup>+</sup>, FGFR3<sup>-</sup>, Ran 2<sup>-</sup>. These cells can develop ''in vitro'' from the either tripotential GRP (probably via O2A stage) or from bipotential O2A cells (which some people think may in turn have been derived from the GRP) '''or''' in vivo when the these progenitor cells are '''transplanted''' into lesion sites (but ''probably not in normal development, at least not in the rat optic nerve''). Type-2 astrocytes are the major astrocytic component in postnatal optic nerve cultures that are generated by O2A cells grown in the presence of fetal calf serum but are not thought to exist in vivo (Fulton et al. | * Type 2: Antigenically A2B5<sup>+</sup>, GFAP<sup>+</sup>, FGFR3<sup>-</sup>, Ran 2<sup>-</sup>. These cells can develop ''in vitro'' from the either tripotential GRP (probably via O2A stage) or from bipotential O2A cells (which some people think may in turn have been derived from the GRP) '''or''' in vivo when the these progenitor cells are '''transplanted''' into lesion sites (but ''probably not in normal development, at least not in the rat optic nerve''). Type-2 astrocytes are the major astrocytic component in postnatal optic nerve cultures that are generated by O2A cells grown in the presence of fetal calf serum but are not thought to exist in vivo (Fulton et al. 1992). | ||
'''(2) Anatomically | |||
* | *Protoplasmic: found in [[grey matter]] and have many branching processes whose end-feet envelop [[synapses]]. Some protoplasmic astrocytes are generated by multipotent [[subventricular zone]] progenitor cells. <ref name="pmid8439409">{{cite journal |author=Levison SW, Goldman JE |title=Both oligodendrocytes and astrocytes develop from progenitors in the subventricular zone of postnatal rat forebrain |journal=Neuron |volume=10 |pages=201–12 |year=1993 |pmid=8439409 }}</ref><ref>{{cite journal |author=Zerlin M ''et al.'' |title=Early patterns of migration, morphogenesis, and intermediate filament expression of subventricular zone cells in the postnatal rat forebrain |journal=J Neurosci |volume=15 |pages=7238–49 |year=1995 |pmid=7472478 }}</ref> | ||
- | *Fibrous: found in [[white matter]], these have long thin unbranched processes whose end-feet envelop [[nodes of Ranvier]].<ref>{{MUNAnatomy|nerve/neuron}}</ref> Some fibrous astrocytes are generated by [[radial glia]]. <ref name="pmid77708">{{cite journal |author=Choi BH, Lapham LW |title=Radial glia in the human fetal cerebrum: a combined Golgi, immunofluorescent and electron microscopic study |journal=Brain Res |volume=148 |pages=295–311 |year=1978 |pmid=77708}}</ref><ref name="pmid111580">{{cite journal |author=Schmechel DE, Rakic P |title=A Golgi study of radial glial cells in developing monkey telencephalon: morphogenesis and transformation into astrocytes |journal=Anat Embryol |volume=156 |pages=115–52 |year=1979 |pmid=111580}}</ref><ref>{{cite journal |author=Misson JP ''et al.''|title=Identification of radial glial cells within the developing murine central nervous system: studies based upon a new immunohistochemical marker |journal=Brain Res |volume=44 |pages=95–108 |year=1988 |pmid=3069243 }}</ref><ref name="pmid2808761">{{cite journal |author=Voigt T |title=Development of glial cells in the cerebral wall of ferrets: direct tracing of their transformation from radial glia into astrocytes |journal=J Comp Neurol |volume=289 |pages=74–88 |year=1989 |pmid=2808761}}</ref><ref>{{cite journal |author=Goldman SA ''et al.'' |title=Ependymal/subependymal zone cells of postnatal and adult songbird brain generate both neurons and nonneuronal siblings in vitro and in vivo |journal=J Neurobiol |volume=30|pages=505–20 |year=1996|pmid=8844514 }}</ref> | ||
'''(3) By Transporter/receptor classification''' | '''(3) By Transporter/receptor classification''' | ||
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==Bergmann glia== | ==Bergmann glia== | ||
''Bergmann glia'' | ''Bergmann glia''<ref>{{cite journal |author=Riquelme R ''et al.'' |title=Bergmann glia GABA(A) receptors concentrate on the glial processes that wrap inhibitory synapses |journal=J. Neurosci |volume=22 |pages=10720–30 |year=2002 |pmid=12486165 |url=http://www.jneurosci.org/cgi/content/abstract/22/24/10720 }}</ref><ref>{{cite journal |author=Yamada K, Watanabe M |title=Cytodifferentiation of Bergmann glia and its relationship with Purkinje cells |journal=Anat Sci Int |volume=77 |pages=94–108 |year=2002 |pmid=12418089}}</ref> also known as radial epithelial cells (as named by [[Camillo Golgi]]), are astrocytes in the [[cerebellum]] that have their [[cell body|cell bodies]] in the [[Purkinje cell]] layer and processes that extend into the molecular layer, terminating with bulbous endfeet at the [[pia mater|pial]] surface. Bergmann glia express high densities of glutamate transporters that limit diffusion of the glutamate during its release from synaptic terminals. Besides their role in early development of the cerebellum, Bergmann glia are also required for the pruning or addition of [[synapse]]s. | ||
==Pathology== | ==Pathology== | ||
| Line 63: | Line 55: | ||
==References== | ==References== | ||
<references/> | |||
Revision as of 07:06, 24 May 2011
Astrocytes (or astroglia) are star-shaped glial cells in the brain and spinal cord. They have many functions, including biochemical support of epithelial cells that form the blood-brain barrier, the provision of nutrients to the nervous tissue, and thay have a major role in the repair and scarring process in the brain. They also intercommunicate with neurones, and have an important role in the uptake and degradation of neurotransmitters released by neurons into the extracellular space.
Description
Astrocytes are a sub-type of the glial cells. Their primary processes are star-shaped, and numerous fine processes largely fill the space between the "star beams" to create a spongiform shape. Fine distal processes of the astrocyte envelop, or "ensheath" neurons and their axons. Proximity and interaction between synaptic elements and astrocytic processes gave rise to a concept of "tripartite synapse"[1]. The degree of synapse ensheathing varies between brain areas and between individual synapses, and it can also change in an activity-dependent manner, allowing for structural plasticity of tripartite synapse. Astrocytes express many different receptors for peptides and other signalling molecules that are released by neurons, and these signals regulate their shape and function.
Classically, astrocytes are identified histologically by their expression of the intermediate filament glial fibrillary acidic protein (GFAP), although the level of GFAP expression varies widely between astrocytes. Two forms of astrocytes exist in the CNS, fibrous and protoplasmic. Fibrous astrocytes are usually located within white matter, have relatively few organelles, and have long, unbranched processes. This type often has "vascular feet", also called endfeet, that connect the astrocyte to the outside of capillary wall. Protoplasmic astrocytes, found in grey matter, have more organelles, and short,highly branched processes. When in proximity to the pia mater, astrocytes send out their processes to form the pia-glial membrane.
Formerly, astrocytes were looked upon as gap fillers in the CNS, playing essentially a supportive, structural role. However, astrocytic networks are now thought to play a number of active roles in the brain, including the secretion and uptake of neurotransmitters, "siphoning" K+ ions away from synapses, regulation of synaptogenesis, modulation of synaptic transmission, short- and long-term synaptic plasticity, neuro-vascular coupling, maintenance of the blood-brain barrier and more.
Functions
- Structural: involved in the physical structuring of the brain.
- Metabolic support: providing neurons with nutrients such as glucose.
- Blood-brain barrier: the astrocyte end-feet encircling endothelial cells were thought to aid in the maintenance of the blood-brain barrier, but recent research indicates that the tight junctions and basal lamina of the cerebral endothelial cells that play the most substantial role in maintaining the barrier.
- Transmitter reuptake and release: astrocytes express plasma membrane transporters such as glutamate transporters for several neurotransmitters, including glutamate, ATP and GABA. More recently, astrocytes have been shown shown to release glutamate or ATP in a vesicular, Ca2+-dependent manner.[2][3]
- Regulation of ion concentration in the extracellular space: astrocytes express potassium channels at a high density. When neurons are active, they release potassium, increasing the local extracellular concentration. Because astrocytes are highly permeable to potassium, they rapidly clear the excess accumulation in the extracellular space. If this function is interfered with, the extracellular concentration of potassium will rise, leading to neuronal depolarization by the Goldman equation. Abnormal accumulation of extracellular potassium can result in epileptic neuronal activity.
- Modulation of synaptic transmission: in the supraoptic nucleus of the hypothalamus, rapid changes in the morphology of astrocytes occur in a variety of different physiological states, including lactation. These changes been shown to affect heterosynaptic transmission between neurons.[4]
- Vasomodulation: astrocytes may serve as intermediaries in neuronal regulation of blood flow.[5]
- Promotion of the myelinating activity of oligodendrocytes: electrical activity in neurons causes them to release ATP, which serves as an important stimulus for myelin to form. Surprisingly, ATP does not act directly on oligodendrocytes; instead it causes astrocytes to secrete the cytokine leukemia inhibitory factor, a regulatory protein that promotes the myelinating activity of oligodendrocytes. [6]
- Nervous system repair: upon injury to nerve cells , astrocytes become phagocytic to ingest the injured nerve cells. The astrocytes then fill up the space to form a glial scar, repairing the area and replacing the CNS cells that cannot regenerate.
Astrocytes are important in regulating neural stem cells. The human brain contains numerous neural stem cells, which are kept in a dormant state by chemical signals (ephrin-A2 and ephrin-A3) from the astrocytes. Astrocytes can activate the stem cells to transform into working neurons by dampening the release of ephrin-A2 and ephrin-A3.
Calcium waves
Astrocytes are linked by gap junctions, creating an electrically coupled syncytium.[7] Waves of intracellular calcium can propagate outwards through this syncytium. Mechanisms of calcium wave propagation include diffusion of IP3 through gap junctions and extracellular ATP signalling.[8] Calcium elevations are the primary known axis of activation in astrocytes, and are necessary and sufficient for some types of astrocytic glutamate release.[9]
Classification
There are several ways to classify astrocytes: (1) By lineage and antigenic phenotype from the classic studies of Raff et al. on rat optic nerves.
- Type 1: Antigenically Ran2+, GFAP+, FGFR3+, A2B5- thus resembling the "type 1 astrocyte" of the postnatal day 7 rat optic nerve. These can arise from the tripotential glial restricted precursor cells (GRP), but not from the bipotential O2A/OPC (oligodendrocyte, type 2 astrocyte precursor, also called Oligodendrocye progenitor cell) cells.
- Type 2: Antigenically A2B5+, GFAP+, FGFR3-, Ran 2-. These cells can develop in vitro from the either tripotential GRP (probably via O2A stage) or from bipotential O2A cells (which some people think may in turn have been derived from the GRP) or in vivo when the these progenitor cells are transplanted into lesion sites (but probably not in normal development, at least not in the rat optic nerve). Type-2 astrocytes are the major astrocytic component in postnatal optic nerve cultures that are generated by O2A cells grown in the presence of fetal calf serum but are not thought to exist in vivo (Fulton et al. 1992).
(2) Anatomically
- Protoplasmic: found in grey matter and have many branching processes whose end-feet envelop synapses. Some protoplasmic astrocytes are generated by multipotent subventricular zone progenitor cells. [10][11]
- Fibrous: found in white matter, these have long thin unbranched processes whose end-feet envelop nodes of Ranvier.[12] Some fibrous astrocytes are generated by radial glia. [13][14][15][16][17]
(3) By Transporter/receptor classification
- GluT type: express glutamate transporters (EAAT1/Template:Gene and EAAT2/Template:Gene) and respond to synaptic release of glutamate by transporter currents
- GluR type: express glutamate receptors (mostly mGluR and AMPA type) and respond to synaptic release of glutamate by channel-mediated currents and IP3-dependent Ca2+ transients
Bergmann glia
Bergmann glia[18][19] also known as radial epithelial cells (as named by Camillo Golgi), are astrocytes in the cerebellum that have their cell bodies in the Purkinje cell layer and processes that extend into the molecular layer, terminating with bulbous endfeet at the pial surface. Bergmann glia express high densities of glutamate transporters that limit diffusion of the glutamate during its release from synaptic terminals. Besides their role in early development of the cerebellum, Bergmann glia are also required for the pruning or addition of synapses.
Pathology
Astrocytomas are primary intracranial tumors derived from astrocyte cells of the brain. Under the 1993 World Health Association criteria, a glioblastoma can be considered a "high-grade" (Grade IV) astrocytoma; grade III anaplastic astrocytomas are also malignant. The lower-grade astrocytomas may progress to higher-grade [20]
References
- ↑ Araque A et al. (1999). "Tripartite synapses: glia, the unacknowledged partner". Trends Neurosci. 22: 208–15. PMID 10322493.
- ↑ Santello M, Volterra A (2008). "Synaptic modulation by astrocytes via Ca(2+)-dependent glutamate release.". Neuroscience Mar 22. PMID 18455880.
- ↑ Pryazhnikov E, Khiroug L. (2008). "Synaptic Sub-micromolar increase in [Ca(2+)](i) triggers delayed exocytosis of ATP in cultured astrocytes.". Glia 56:38-49.. PMID 17910050.
- ↑ Piet R et al. (2004). "Physiological contribution of the astrocytic environment of neurons to intersynaptic crosstalk". Proc Natl Acad Sci U S A 101: 2151–5. PMID 14766975.
- ↑ Parri R, Crunelli V (2003). "An astrocyte bridge from synapse to blood flow". Nat Neurosci 6: 5–6. PMID 12494240.
- ↑ Ishibashi T et al. (2006). "Astrocytes promote myelination in response to electrical impulses". Neuron 49: 823–32. PMID 16543131.
- ↑ Bennett M et al. (2003). "New roles for astrocytes: gap junction hemichannels have something to communicate". Trends Neurosci 26: 610–7. PMID 14585601.
- ↑ Newman, J (2001) Neuroscience 21:2215-23
- ↑ Parpura V, Haydon P (2000). "Physiological astrocytic calcium levels stimulate glutamate release to modulate adjacent neurons". Proc Natl Acad Sci U S A 97: 8629–34. PMID 10900020.
- ↑ Levison SW, Goldman JE (1993). "Both oligodendrocytes and astrocytes develop from progenitors in the subventricular zone of postnatal rat forebrain". Neuron 10: 201–12. PMID 8439409.
- ↑ Zerlin M et al. (1995). "Early patterns of migration, morphogenesis, and intermediate filament expression of subventricular zone cells in the postnatal rat forebrain". J Neurosci 15: 7238–49. PMID 7472478.
- ↑ Template:MUNAnatomy
- ↑ Choi BH, Lapham LW (1978). "Radial glia in the human fetal cerebrum: a combined Golgi, immunofluorescent and electron microscopic study". Brain Res 148: 295–311. PMID 77708.
- ↑ Schmechel DE, Rakic P (1979). "A Golgi study of radial glial cells in developing monkey telencephalon: morphogenesis and transformation into astrocytes". Anat Embryol 156: 115–52. PMID 111580.
- ↑ Misson JP et al. (1988). "Identification of radial glial cells within the developing murine central nervous system: studies based upon a new immunohistochemical marker". Brain Res 44: 95–108. PMID 3069243.
- ↑ Voigt T (1989). "Development of glial cells in the cerebral wall of ferrets: direct tracing of their transformation from radial glia into astrocytes". J Comp Neurol 289: 74–88. PMID 2808761.
- ↑ Goldman SA et al. (1996). "Ependymal/subependymal zone cells of postnatal and adult songbird brain generate both neurons and nonneuronal siblings in vitro and in vivo". J Neurobiol 30: 505–20. PMID 8844514.
- ↑ Riquelme R et al. (2002). "Bergmann glia GABA(A) receptors concentrate on the glial processes that wrap inhibitory synapses". J. Neurosci 22: 10720–30. PMID 12486165.
- ↑ Yamada K, Watanabe M (2002). "Cytodifferentiation of Bergmann glia and its relationship with Purkinje cells". Anat Sci Int 77: 94–108. PMID 12418089.
- ↑ Stephen B. Tatter (2006), The new WHO Classification of Tumors affecting the Central Nervous System, Neurosurgical Service, Massachussetts General Hospital