Astrocyte: Difference between revisions

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* '''Metabolic support''': they provide neurons with nutrients such as [[glucose]].
* '''Metabolic support''': they provide 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 they do not play a substantial role; instead it is the [[tight junctions]] and [[basal lamina]] of the cerebral endothelial cells that play the most substantial role in maintaining the barrier.{{Fact|date=January 2008}}
* '''[[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 they do not play a substantial role; instead it is the [[tight junctions]] and [[basal lamina]] of the cerebral endothelial cells that play the most substantial role in maintaining the barrier.{{Fact|date=January 2008}}
* '''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 were 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 | doi = 10.1016/j.neuroscience.2008.03.039 </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 = Jan 1;56(1):38-49. | year = 2008 | pmid = 17910050 | doi = 10.1002/glia.20590 </ref>}}
* '''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 were 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 | doi = 10.1016/j.neuroscience.2008.03.039}} </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 = Jan 1;56(1):38-49. | year = 2008 | pmid = 17910050 | doi = 10.1002/glia.20590}} </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 is well known to result in epileptic neuronal activity.{{Fact|date=January 2008}}
* '''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 is well known to result in epileptic neuronal activity.{{Fact|date=January 2008}}

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Astrocytes (also known collectively as astroglia) are characteristic star-shaped glial cells in the brain and spinal cord. They perform many functions, including biochemical support of endothelial cells which form the blood-brain barrier, the provision of nutrients to the nervous tissue, and a principal role in the repair and scarring process in the brain.

Description

Astrocytes are a sub-type of the glial cells in the brain and spinal cord. They are also known as astrocytic glial cells. The primary processes of an astrocyte are star-shaped, hence the name; however, the numerous fine processes envelope synaptic connections formed between neurons. Astrocytes are classically identified histologically as many of these cells express the intermediate filament glial fibrillary acidic protein (GFAP). Two forms of astrocytes exist in the CNS, fibrous and protoplasmic. The former is usually located within white matter, have relatively few organelles, and exhibit long unbranched cellular processes. This type often have "vascular feet" that physically connect the cells to the outside of capillary wall when they are in close proximity of them. The latter, found in grey matter tissue, possess a larger quantity of organelles, and exhibit short and highly branched cellular processes. The two forms of astrocytes when in proximity to the pia mater sends out process to form the pia-glial membrane.

Previously in medical science, the neuronal network was considered the only important one, and astrocytes were looked upon as gap fillers. But recently they have been reconsidered, and are now thought to play a number of active roles in the brain, including the secretion or absorption of neural transmitters and maintenance of the blood-brain barrier.

Functions

  • Structural: involved in the physical structuring of the brain.
  • Metabolic support: they provide 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 they do not play a substantial role; instead it is the tight junctions and basal lamina of the cerebral endothelial cells that play the most substantial role in maintaining the barrier.Template:Fact
  • Transmitter reuptake and release: astrocytes express plasma membrane transporters such as glutamate transporters for several neurotransmitters, including glutamate, ATP and GABA. More recently, astrocytes were shown to release glutamate or ATP in a vesicular, Ca2+-dependent manner.{{[1]}}{{[2]}}
  • 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 is well known to result in epileptic neuronal activity.Template:Fact
  • Modulation of synaptic transmission: in the supraoptic nucleus of the hypothalamus, rapid changes in astrocyte morphology have been shown to affect heterosynaptic transmission between neurons.[3]
  • Vasomodulation: astrocytes may serve as intermediaries in neuronal regulation of blood flow.[4]
  • 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, the ATP does not act directly on oligodendrocytes. Instead it causes astrocytes to secrete cytokine leukemia inhibitory factor (LIF), a regulatory protein that promotes the myelinating activity of oligodendrocytes. This suggest that astrocytes have an executive-coordinating role in the brain.[5]
  • Nervous system repair: upon injury to nerve cells within the central nervous system, 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.Template:Fact

Recent studies have shown that astrocytes play an important function in the regulation of neural stem cells. Research from the Schepens Eye Research Institute at Harvard shows the human brain to abound in neural stem cells, which are kept in a dormant state by chemical signals (ephrin-A2 and ephrin-A3) from the astrocytes. The astrocytes are able to activate the stem cells to transform into working neurons by dampening the release of ephrin-A2 and ephrin-A3.Template:Fact

Furthermore, studies are underway to determine whether astroglia play an instrumental role in depression, based on the link between diabetes and depression. Altered CNS glucose metabolism is seen in both these conditions, and the astroglial cells are the only cells with insulin receptors in the brain.

Calcium waves

Astrocytes are linked by gap junctions, creating an electrically coupled syncytium.[6]

An increase in intracellular calcium concentration can propagate outwards through this syncytium. Mechanisms of calcium wave propagation include diffusion of IP3 through gap junctions and extracellular ATP signalling.[7] Calcium elevations are the primary known axis of activation in astrocytes, and are necessary and sufficient for some types of astrocytic glutamate release.[8]


Classification

There are several different ways to classify astrocytes:

by Lineage and antigenic phenotype

These have been established by classic work by Raff et al in early 1980s 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).

by Anatomical Classification

by Transporter/receptor classification

Bergmann glia

Bergmann glia, a type of glia[17][18] 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 neurotransmitter 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.citation needed

Pathology

Astrocytomas are primary intracranial tumors derived from astrocytes cells of the brain.

References

  1. ↑ Santello M, Volterra A (2008). "Synaptic modulation by astrocytes via Ca(2+)-dependent glutamate release.". Neuroscience Mar 22. DOI:10.1016/j.neuroscience.2008.03.039. PMID 18455880. Research Blogging.
  2. ↑ Pryazhnikov E, Khiroug L. (2008). "Synaptic Sub-micromolar increase in [Ca(2+)](i) triggers delayed exocytosis of ATP in cultured astrocytes.". Glia. Jan 1;56(1):38-49.. DOI:10.1002/glia.20590. PMID 17910050. Research Blogging.
  3. ↑ Piet R, Vargová L, Syková E, Poulain D, Oliet S (2004). "Physiological contribution of the astrocytic environment of neurons to intersynaptic crosstalk". Proc Natl Acad Sci U S A 101 (7): 2151–5. DOI:10.1073/pnas.0308408100. PMID 14766975. Research Blogging.
  4. ↑ Parri R, Crunelli V (2003). "An astrocyte bridge from synapse to blood flow". Nat Neurosci 6 (1): 5–6. DOI:10.1038/nn0103-5. PMID 12494240. Research Blogging.
  5. ↑ Ishibashi T, Dakin K, Stevens B, Lee P, Kozlov S, Stewart C, Fields R (2006). "Astrocytes promote myelination in response to electrical impulses". Neuron 49 (6): 823–32. DOI:10.1016/j.neuron.2006.02.006. PMID 16543131. Research Blogging.
  6. ↑ Bennett M, Contreras J, Bukauskas F, Sáez J (2003). "New roles for astrocytes: gap junction hemichannels have something to communicate". Trends Neurosci 26 (11): 610–7. DOI:10.1016/j.tins.2003.09.008. PMID 14585601. Research Blogging.
  7. ↑ Newman, J Neurosci. 2001 Apr 1;21(7):2215-23
  8. ↑ Parpura V, Haydon P (2000). "Physiological astrocytic calcium levels stimulate glutamate release to modulate adjacent neurons". Proc Natl Acad Sci U S A 97 (15): 8629–34. DOI:10.1073/pnas.97.15.8629. PMID 10900020. Research Blogging.
  9. ↑ Levison SW, Goldman JE (February 1993). "Both oligodendrocytes and astrocytes develop from progenitors in the subventricular zone of postnatal rat forebrain". Neuron 10 (2): 201–12. PMID 8439409. [e]
  10. ↑ Zerlin M, Levison SW, Goldman JE (November 1995). "Early patterns of migration, morphogenesis, and intermediate filament expression of subventricular zone cells in the postnatal rat forebrain". J. Neurosci. 15 (11): 7238–49. PMID 7472478. [e]
  11. ↑ Template:MUNAnatomy
  12. ↑ Choi BH, Lapham LW (June 1978). "Radial glia in the human fetal cerebrum: a combined Golgi, immunofluorescent and electron microscopic study". Brain Res. 148 (2): 295–311. PMID 77708. [e]
  13. ↑ Schmechel DE, Rakic P (June 1979). "A Golgi study of radial glial cells in developing monkey telencephalon: morphogenesis and transformation into astrocytes". Anat. Embryol. 156 (2): 115–52. PMID 111580. [e]
  14. ↑ Misson JP, Edwards MA, Yamamoto M, Caviness VS (November 1988). "Identification of radial glial cells within the developing murine central nervous system: studies based upon a new immunohistochemical marker". Brain Res. Dev. Brain Res. 44 (1): 95–108. PMID 3069243. [e]
  15. ↑ Voigt T (November 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 (1): 74–88. DOI:10.1002/cne.902890106. PMID 2808761. Research Blogging.
  16. ↑ Goldman SA, Zukhar A, Barami K, Mikawa T, Niedzwiecki D (August 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 (4): 505–20. DOI:<505::AID-NEU6>3.0.CO;2-7 10.1002/(SICI)1097-4695(199608)30:4<505::AID-NEU6>3.0.CO;2-7. PMID 8844514. <505::AID-NEU6>3.0.CO;2-7 Research Blogging.
  17. ↑ Riquelme R, Miralles C, De Blas A (2002). "Bergmann glia GABA(A) receptors concentrate on the glial processes that wrap inhibitory synapses". J. Neurosci. 22 (24): 10720–30. PMID 12486165.
  18. ↑ Yamada K, Watanabe M (2002). "Cytodifferentiation of Bergmann glia and its relationship with Purkinje cells". Anatomical science international / Japanese Association of Anatomists 77 (2): 94–108. PMID 12418089.
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