Astrocyte

Astrocytes (Astro from Greek astron = star and cyte from Greek "kytos" =
Astrocyte
cavity but also means cell), also known collectively as astroglia, are
characteristic star-shaped glial cells in the brain and spinal cord. The proportion
of astrocytes in the brain is not well defined. Depending on the counting
technique used, studies have found that the astrocyte proportion varies by region
and ranges from 20% to 40% of all glia.[1] They perform many functions,
including biochemical support of endothelial cells that form the blood–brain
barrier, provision of nutrients to the nervous tissue, maintenance of extracellular
ion balance, and a role in the repair and scarring process of the brain and spinal
cord following traumatic injuries.

Research since the mid-1990s has shown that astrocytes propagate intercellular An astrocytic cell from rat brain grown in
Ca2+ waves over long distances in response to stimulation, and, similar to tissue culture and stained with
neurons, release transmitters (called gliotransmitters) in a Ca2+-dependent antibodies to GFAP (red) and vimentin
manner. Data suggest that astrocytes also signal to neurons through Ca2+- (green). Both proteins are present in
dependent release of glutamate.[2] Such discoveries have made astrocytes an large amounts in the intermediate
important area of research within the field ofneuroscience. filaments of this cell, so the cell appears
yellow. The blue material shows DNA
visualized with DAPI stain, and reveals
the nuclei of the astrocyte and other
Contents cells. Image courtesy of EnCor
Biotechnology Inc.
Structure
Development Details

Function Identifiers
Bergmann glia Latin Astrocytus
Tripartite synapse
MeSH D001253
Clinical significance
Astrocytomas NeuroLex sao1394521419
Neurodevelopment disorders ID
Chronic pain TH H2.00.06.2.00002,
Two states of persistent pain
H2.00.06.2.01008
Other pathologies
Anatomical terminology
Research
Classification
Lineage and antigenic phenotype
Anatomical classification
Transporter/receptor classification
See also
References
Further reading
External links

Structure
Astrocytes are a sub-type ofglial cells in the central nervous system. They are
also known as astrocytic glial cells. Star-shaped, their many processes
envelop synapses made by neurons. Astrocytes are classically identified using
histological analysis; many of these cells express the intermediate filament
glial fibrillary acidic protein (GFAP).[3] Several forms of astrocytes exist in
the central nervous system including fibrous (in white matter), protoplasmic
(in grey matter), and radial. The fibrous glia are usually located within white
matter, have relatively few organelles, and exhibit long unbranched cellular
processes. This type often has "vascular feet" that physically connect the cells
to the outside of capillary walls when they are in proximity to them. The
protoplasmic glia are the most prevalent and are found in grey matter tissue, Astrocytes (green) in the context of
neurons (red) in a mouse cortexcell culture
possess a larger quantity of organelles, and exhibit short and highly branched
tertiary processes. The radial glia are disposed in planes perpendicular to the
axes of ventricles. One of their processes abuts the pia mater, while the other
is deeply buried in gray matter. Radial glia are mostly present during
development, playing a role in neuron migration. Müller cells of the retina
and Bergmann glia cells of the cerebellar cortex represent an exception, being
present still during adulthood. When in proximity to the pia mater, all three
forms of astrocytes send out processes to form the pia-glial membrane.

Development
Astrocytes are macroglial cells in the central nervous system. Astrocytes are
23-week-old fetal brain culture human
derived from heterogeneous populations of progenitor cells in the
astrocyte
neuroepithelium of the developing central nervous system. There is
remarkable similarity between the well known genetic mechanisms that
specify the lineage of diverse neuron subtypes and that of macroglial cells.[4]
Just as with neuronal cell specification, canonical signaling factors like Sonic
hedgehog (SHH), Fibroblast growth factor (FGFs), WNTs and bone
morphogenetic proteins(BMPs), provide positional information to developing
macroglial cells through morphogen gradients along the dorsal–ventral,
anterior–posterior and medial–lateral axes. The resultant patterning along the
neuraxis leads to segmentation of the neuroepithelium into progenitor
domains (p0, p1 p2, p3 and pMN) for distinct neuron types in the developing
spinal cord. On the basis of several studies it is now believed that this model Astrocytes (red-yellow) among neurons
also applies to macroglial cell specification. Studies carried out by Hochstim (green) in the living cerebral cortex
and colleagues have demonstrated that three distinct populations of astrocytes
arise from the p1, p2 and p3 domains.[5] These subtypes of astrocytes can be
identified on the basis of their expression of different transcription factors (PAX6, NKX6.1) and cell surface markers (reelin and
SLIT1). The three populations of astrocyte subtypes which have been identified are 1) dorsally located VA1 astrocytes, derived from
p1 domain, express PAX6 and reelin 2) ventrally located VA3 astrocytes, derived from p3, express NKX6.1 and SLIT1 and 3) and
intermediate white-matter located VA2 astrocyte, derived from the p2 domain, which express PAX6, NKX6.1, reelin and SLIT1.[6]
After astrocyte specification has occurred in the developing CNS, it is believed that astrocyte precursors migrate to their final
positions within the nervous system before the process of terminaldifferentiation occurs.

Function
Previously in medical science, the neuronal network was considered the only important function of astrocytes, and they were looked
upon as gap fillers. More recently, the function of astrocytes has been reconsidered, and they 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.[8]
Following on this idea the concept of a "tripartite synapse" has been proposed,
referring to the tight relationship occurring at synapses among a presynaptic
[9]
element, a postsynaptic element and a glial element.

Structural: They are involved in the physical structuring of the brain.

Astrocytes get their name because they are "star-shaped". They are the
most abundant glial cells in the brain that are closely associated with
neuronal synapses. They regulate the transmission of electrical
impulses within the brain.
Glycogen fuel reserve buffer: Astrocytes contain glycogen and are
capable of glycogenesis. The astrocytes next to neurons in thefrontal
cortex and hippocampus store and release glycogen. Thus, astrocytes
can fuel neurons with glucose during periods of high rate of glucose
consumption and glucose shortage. Recent research suggests there
may be a connection between this activity and exercise. [10]
Astrocytes are depicted in red. Cell
Metabolic support: They provide neurons with nutrients such as nuclei are depicted in blue.
lactate. Astrocytes were obtained from brains
Blood–brain barrier: The astrocyte end-feet encirclingendothelial cells of newborn mice
were thought to aid in the maintenance of the blood–brain barrier, but
recent research indicates that they do not play a substantial role;

[7]
Metabolic interactions between astrocytes and neurons.

instead, it is the tight junctions and basal lamina of the cerebral endothelial cells that play the most substantial role in
maintaining the barrier.[11] However, it has recently been shown that astrocyte activity is linked to blood flow in the
brain, and that this is what is actually being measured in fMRI. [12][13]

Transmitter uptake and release: Astrocytes express plasma membrane transporters such asglutamate
transporters for several neurotransmitters, includingglutamate, ATP, and GABA. More recently, astrocytes were
shown to release glutamate orATP in a vesicular, Ca2+-dependent manner.[14] (This has been disputed for
hippocampal astrocytes.)[15]
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.[16] 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.[17]
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.[18] In the hippocampus,
astrocytes suppress synaptic transmission by releasing T
AP, which is hydrolyzed by ectonucleotidases to yield
adenosine. Adenosine acts on neuronaladenosine receptors to inhibit synaptic transmission, thereby increasing the
dynamic range available for LTP.[19]
Vasomodulation: Astrocytes may serve as intermediaries in neuronal regulation of blood flow .[20]
Promotion of the myelinating activity ofoligodendrocytes: Electrical activity in neurons causes them to release
ATP, which serves as an important stimulus or f myelin to form. However, 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 suggests that astrocytes have an executive-
coordinating role in the brain.[21]
Nervous system repair: Upon injury to nerve cells within the central nervous system, astrocytes fill up the space to
form a glial scar, and may contribute to neural repair. The role of astrocytes in CNS regeneration following injury is
not well understood though. The glial scar has traditionally been described as an impermeable barrier to
regeneration, thus implicating a negative role in axon regeneration. However , recently, it was found through genetic
ablation studies that astrocytes are actually required for regeneration to occur .[22] Even more exciting, these authors
found that the astrocyte scar is actually essential for stimulated axons (that axons that have been coaxed to grow via
neurotrophic supplementation) to extend through the injured spinal cord. [22] Interestingly, astrocytes that have been
pushed into a reactive phenotype (termed astrogliosis, defined by upregulation of GF AP expression, a definition still
under debate) may actually be toxic to neurons, releasing signals that can kill neurons. [23] Much work, however,
remains to elucidate their role in nervous system injury .
Long-term potentiation: Scientists debate whether astrocytes integrate learning and memory in the hippocampus.
Recently it has been shown that engrafting human glial progenitor cell in the nascent mice brains will cause the cells
to differentiate into astrocytes. After differentiation these cells increase LTP and improve memory performance in the
mice.[24]
The switch of the nervous system: Based on the evidence listed below, it has been recently conjectured in,[25] that
macro glia (and astrocytes in particular) act both as a lossy neurotransmitter capacitor and as the logical switch of
the nervous system. I.e., macroglia either block or enable the propagation of the stimulus along the nervous system,
depending on their membrane state and the level of the stimulus.

Fig. 6 The conjectured switching role of glia in the biological neural detection scheme as suggested by
Nossenson et al [25][26]
 Evidence type Description References

Calcium evidence | [27][28][29]

A negative wave appears when the stimulus level crosses a certain threshold.
Electrophysiological The shape of the electrophysiological response is dif
ferent and has the [30][31][32]
evidence opposite polarity compared to the characteristic neural response, suggesting
that cells other than neurons might be involved.
The negative electrophysiological response is accompanied with all-or-none
Psychophysical actions. A moderate negative electrophysiological response appears in
Evidence conscious logical decisions such as perception tasks. An intense sharp
negative wave appear in epileptic seizures and during reflexes.
Radioactivity based Glutamate uptake tests indicate on a saturation level after which
glutamate uptake neurotransmitter uptake level stops rising proportionally to neurotransmitter [33]
tests concentration.

Astrocytes are linked by gap junctions, creating an electrically coupled (functional) syncytium.[34] Because of this ability of
astrocytes to communicate with their neighbors, changes in the activity of one astrocyte can have repercussions on the activities of
others that are quite distant from the original astrocyte.

An influx of Ca2+ ions into astrocytes is the essential change that ultimately generates calcium waves. Because this influx is directly
caused by an increase in blood flow to the brain, calcium waves are said to be a kind of hemodynamic response function. An increase
in intracellular calcium concentration can propagate outwards through this functional syncytium. Mechanisms of calcium wave
propagation include diffusion of calcium ions and IP3 through gap junctions and extracellular ATP signalling.[35] Calcium elevations
are the primary known axis of activation in astrocytes, and are necessary and sufficient for some types of astrocytic glutamate
release.[36] Given the importance of calcium signaling in astrocytes, tight regulatory mechanisms for the progression of the spatio-
temporal calcium signaling have been developed. Via mathematical analysis it has been shown that localized inflow of Ca2+ ions
yields a localized raise in the cytosolic concentration of Ca2+ ions.[37] Moreover, cytosolic Ca2+ accumulation is independent of
every intracellular calcium flux and depends on the Ca2+ exchange across the membrane, cytosolic calcium diffusion, geometry of
[37]
the cell, extracellular calcium perturbation, and initial concentrations.

Bergmann glia
Bergmann glia, a type of glia[38][39] also known as radial epithelial cells (as named by
Camillo Golgi) or Golgi epithelial cells (GCEs; not to be mixed up with Golgi cells)or
due to lack of ependymal processes should be called radially oriented astrocytes,[40] are
astrocytes in the cerebellum that have their cell bodies in the Purkinje cellAvg. 3-6 cell
per Purkinje layer[41] and processes that extend into the molecular layer, terminating
with bulbous endfeet at the pial surface. Bergmann glial cells form rows or palisades
that are aligned to the long axis of folium characterized by high surface to volume ratio
up to 20 micro-meters in rodent cerebellum there are 8 Ber
gmann glial cells per Purkinje
Cell it has been estimated that each BGC operates around 2000-6000 Purkinje cell
synapses. They occupy around 15%-18% of the molecular layer in cerebellum. The size
and shape differ dependence on animal species thus length of molecular layer which we SLC1A3 expression highlights
call adaptive growth of astroglial cell processes. The Length of processes is determined Bergmann glia in the brain of a
mouse at 7th postnatal day,
by the molecular layer in humans for example the processes are longer but show less
sagittal section.
dense lateral outgrow. the Bergman glia has sub-type called Fanana cells which are
located rather in with somata located in molecular layer.[42] Bergmann glia express high
densities of glutamate transportersthat limit diffusion of the neurotransmitter glutamate during its release from synaptic terminals.[43]
Besides their role in early development of the cerebellum for example Bergman glia are one of main contributors of neuronal
migration in cerebellum of the granule cell neurons using Shh(sonic hedgehog) and cell cycle genes as D2-cyclin,PP2A and the cell
specification of granule cell neurons by activating Notch2 and Jagged2 receptors, these processes extends along whole
cerebellum,[44] Bergmann glia are also required for the pruning or addition of synapses.[45] Bergmann glia form micro-domain
topology which are used as “repetitive units” on the stem of Purkinje Cells processes ,each micro-domain consists of thin stalk and
cabbagelike head structure that bears lamellar perisynaptic sheaths around about 5 synapses these micro-domains may interact with
synapses independently of each other also of the stem processes. The micro domains overlap in every given volume unit of the
molecular layer at least 2 micro-domains originate from different Bergmann glia this fit to the observation that Purkinje cells express
[46]
2 functionally distinct populations of synaptic spines ,and individual spines are capable of independent activation.

Tripartite synapse
Within the dorsal horn of thespinal cord, activated astrocytes have the ability to respond to almost all neurotransmitters[47] and, upon
activation, release a multitude of neuroactive molecules such as glutamate, ATP, nitric oxide (NO), prostaglandins (PG), which in
turn influences neuronal excitability. The close association between astrocytes and presynaptic and postsynaptic terminals as well as
their ability to integrate synaptic activity and release neuromodulators has been termed the "tripartite synapse".[9] Synaptic
modulation by astrocytes takes place because of this 3-part association.

Clinical significance

Astrocytomas
Astrocytomas are primary intracranial tumors derived from astrocytes cells of the brain. It is also possible that glial progenitors or
neural stem cells give rise to astrocytomas.

Astrocytomas are brain tumors that develop from astrocytes. They may occur in many parts of the brain and sometimes in the spinal
cord. They can occur at any age and they primarily occur in males. Astrocytomas are divided into two categories: Low grade (I and
II) and High Grade (III and IV). Low grade tumors are more common in children and high grade tumors are more common in
adults.[48]

Pilocytic astrocytoma are Grade I tumors. They are considered benign and slow growing tumors. Pilocytic astrocytomas frequently
have cystic portions filled with fluid and a nodule, which is the solid portion. Most are located in the cerebellum. Therefore, most
ficulties.[48] They also occur more frequently in children and teens.
symptoms are related to balance or coordination dif [49]

Grade II Tumors grow relatively slow but invade surrounding healthy tissue. Usually considered benign but can grow into malignant
tumors. Other names that are used are Fibrillary or Protoplasmic astrocytomas. They are prevalent in younger people who are often
present with seizures.[49]

Anaplastic astrocytoma is classified as grade III and are malignant tumors. They grow more rapidly than lower grade tumors and tend
to invade nearby healthy tissue. Anaplastic astrocytomas recur more frequently than lower grade tumors because their tendency to
spread into surrounding tissue makes them difficult to completely remove surgically.[48]

Glioblastoma Multiforme is also a malignant tumor and classified as a grade IV. Glioblastomas can contain more than one cell type
(i.e., astrocytes, oligodendrocytes). Also, while one cell type may die off in response to a particular treatment, the other cell types
may continue to multiply. Glioblastomas are the most invasive type of glial tumors as they grow rapidly and spread to nearby tissue.
ficult to treat.[48]
Approximately 50% of astrocytomas are glioblastomas and are very dif

Neurodevelopment disorders
A relatively new direction has emerged in the field of neurodevelopmental disorders. This view states that astrocyte dysfunction may
play a role in the aberration of neuronal circuitry that underlies certain psychiatric disorders, including the autism spectrum disorders
(ASDs) and schizophrenia.[50][51]

Chronic pain
Under normal conditions, pain conduction begins with some noxious signal followed by an action potential carried by nociceptive
(pain sensing) afferent neurons, which elicit excitatory postsynaptic potentials (EPSP) in the dorsal horn of the spinal cord. That
message is then relayed to the cerebral cortex, where we translate those EPSPs into "pain." Since the discovery of astrocytic
influence, our understanding of the conduction of pain has been dramatically complicated. Pain processing is no longer seen as a
repetitive relay of signals from body to brain, but as a complex system that can be up- and down-regulated by a number of different
factors. One factor at the forefront of recent research is in the pain-potentiating synapse located in the dorsal horn of the spinal cord
and the role of astrocytes in encapsulating these synapses. Garrison and co-workers[52] were the first to suggest association when
they found a correlation between astrocyte hypertrophy in the dorsal horn of the spinal cord and hypersensitivity to pain after
peripheral nerve injury, typically considered an indicator of glial activation after injury. Astrocytes detect neuronal activity and can
.[47][53][54] In the past, hyperalgesia was thought to be modulated
release chemical transmitters, which in turn control synaptic activity
by the release of substance P and excitatory amino acids (EAA), such as glutamate, from the presynaptic afferent nerve terminals in
the spinal cord dorsal horn. Subsequent activation of AMPA (α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid), NMDA (N-
methyl-D-aspartate) and kainate subtypes of ionotropic glutamate receptors follows. It is the activation of these receptors that
potentiates the pain signal up the spinal cord. This idea, although true, is an oversimplification of pain transduction. A litany of other
neurotransmitter and neuromodulators, such as calcitonin gene-related peptide (CGRP), adenosine triphosphate (ATP), brain-derived
neurotrophic factor (BDNF), somatostatin, vasoactive intestinal peptide (VIP), galanin, and vasopressin are all synthesized and
released in response to noxious stimuli. In addition to each of these regulatory factors, several other interactions between pain-
transmitting neurons and other neurons in the dorsal horn have added impact on pain pathways.

Two states of persistent pain

After persistent peripheral tissue damage there is a release of several factors from the injured tissue as well as in the spinal dorsal
horn. These factors increase the responsiveness of the dorsal horn pain-projection neurons to ensuing stimuli, termed "spinal
sensitization," thus amplifying the pain impulse to the brain. Release of glutamate, substance P, and calcitonin gene-related peptide
(CGRP) mediates NMDAR activation (originally silent because it is plugged by Mg2+), thus aiding in depolarization of the
postsynaptic pain-transmitting neurons (PTN). In addition, activation of IP3 signaling and MAPKs (mitogen-activated protein
kinases) such as ERK and JNK, bring about an increase in the synthesis of inflammatory factors that alter glutamate transporter
function. ERK also further activates AMPARs and NMDARs in neurons. Nociception is further sensitized by the association of ATP
and substance P with their respective receptors (P2X3) and neurokinin 1 receptor (NK1R), as well as activation of metabotropic
glutamate receptors and release of BDNF. Persistent presence of glutamate in the synapse eventually results in dysregulation of GLT1
and GLAST, crucial transporters of glutamate into astrocytes. Ongoing excitation can also induce ERK and JNK activation, resulting
in release of several inflammatory factors.

As noxious pain is sustained, spinal sensitization creates transcriptional changes in the neurons of the dorsal horn that lead to altered
function for extended periods. Mobilization of Ca2+ from internal stores results from persistent synaptic activity and leads to the
release of glutamate, ATP, tumor necrosis factor-α (TNF-α), interleukin 1β (IL-1β), IL-6, nitric oxide (NO), and prostaglandin E2
(PGE2). Activated astrocytes are also a source of matrix metalloproteinase 2 (MMP2), which induces pro-IL-1β cleavage and
sustains astrocyte activation. In this chronic signaling pathway, p38 is activated as a result of IL-1β signaling, and there is a presence
of chemokines that trigger their receptors to become active. In response to nerve damage, heat shock proteins (HSP) are released and
can bind to their respectiveTLRs, leading to further activation.

Other pathologies
Other clinically significant pathologies involving astrocytes includeastrogliosis and astrocytopathy.[55]

Research
A study performed in November 2010 and published March 2011, was done by a team of scientists from the University of Rochester
and University of Colorado School of Medicine. They did an experiment to attempt to repair trauma to the Central Nervous System
of an adult rat by replacing the glial cells. When the glial cells were injected into the injury of the adult rat’s spinal cord, astrocytes
were generated by exposing human glial precursor cells to bone morphogenetic protein (Bone morphogenetic protein is important
because it is considered to create tissue architecture throughout the body). So, with the bone protein and human glial cells combined,
they promoted significant recovery of conscious foot placement, axonal growth, and obvious increases in neuronal survival in the
spinal cord laminae. On the other hand, human glialprecursor cells and astrocytes generated from these cells by being in contact with
.[56]
ciliary neurotrophic factors, failed to promote neuronal survival and support of axonal growth at the spot of the injury

One study done in Shanghai had two types of hippocampal neuronal cultures: In one culture, the neuron was grown from a layer of
astrocytes and the other culture was not in contact with any astrocytes, but they were instead fed a glial conditioned medium (GCM),
which inhibits the rapid growth of cultured astrocytes in the brains of rats in most cases. In their results they were able to see that
astrocytes had a direct role in Long-term potentiation with the mixed culture (which is the culture that was grown from a layer of
astrocytes) but not in GCM cultures.[57]

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 ofephrin-A2 and ephrin-A3.[58]

In a study published in a 2011 issue of Nature Biotechnology[59] a group of researchers from the University of Wisconsin reports that
it has been able to direct embryonic and induced humanstem cells to become astrocytes.

A 2012 study[60] of the effects of marijuana on short term memories found that THC activates CB1 receptors of astrocytes which
cause receptors for AMPA to be removed from the membranes of associated neurons.

Classification
There are several different ways to classify astrocytes.

Lineage and antigenic phenotype

These have been established by classic work by Raf
f 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 Oligodendrocyte progenitor cell) cells.
Type 2: Antigenically A2B5+, GFAP+, FGFR3−, Ran 2−. These cells can developin vitro from the either tripotential
GRP (probably via O2A stage) or from bipotential O2A cells (which some people{{ [61] }} think may in turn have been
derived from the GRP)or in vivo when 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 astrocyticcomponent 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.[62]

Anatomical classification
Protoplasmic: found ingrey matter and have many branching processes whose end-feet envelopsynapses. Some
protoplasmic astrocytes are generated by multipotentsubventricular zone progenitor cells.[63][64]
Gömöri-positive astrocytes. These are a subset of protoplasmic astrocytes that contain numerous cytoplasmic
inclusions, or granules, that stain positively withGömöri's chrome-alum hematoxylin stain. It is now known that these
granules are formed from the remnants of degenerating mitochondria engulfed within lysosomes, [65] Some type of
oxidative stress appears to be responsible for the mitochondrial damage within these specialized astrocytes.
Gömöri-positive astrocytes are much more abundant within thearcuate nucleus of the hypothalamus and in the
hippocampus than in other brain regions. They may have a role in regulating the response of the hypothalamus to
glucose.[66][67]
Fibrous: found in white matter and have long thin unbranched processes whose end-feet envelopnodes of Ranvier.
Some fibrous astrocytes are generated byradial glia.[68][69][70][71][72]
Transporter/receptor classification
GluT type: these expressglutamate transporters (EAAT1/SLC1A3 and EAAT2/SLC1A2) and respond to synaptic
release of glutamate by transporter currents. The function and availability of EAA
T2 is modulated by TAAR1, an
intracellular receptor in human astrocytes.[73]
GluR type: these expressglutamate receptors (mostly mGluR and AMPA type) and respond to synaptic release of
glutamate by channel-mediated currents andIP3-dependent Ca2+ transients.

See also
Bergmann gliosis
Neuroglia
Pituicyte
Polydendrocytes

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30 (4): 505–20. doi:10.1002/(SICI)1097-4695(199608)30:4<505::AID-NEU6>3.0.CO;2-7(https://doi.org/10.1002%2
F%28SICI%291097-4695%28199608%2930%3A4%3C505%3A%3AAID-NEU6%3E3.0.CO%3B2-7) . PMID 8844514
(https://www.ncbi.nlm.nih.gov/pubmed/8844514).
73. Cisneros IE, Ghorpade A (October 2014)."Methamphetamine and HIV-1-induced neurotoxicity: role of trace amine
associated receptor 1 cAMP signaling in astrocytes"(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4315503).
Neuropharmacology. 85: 499–507. doi:10.1016/j.neuropharm.2014.06.011(https://doi.org/10.1016%2Fj.neurophar
m.2014.06.011). PMC 4315503 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4315503) . PMID 24950453 (http
s://www.ncbi.nlm.nih.gov/pubmed/24950453). "Moreover, TAAR1 overexpression significantly decreased EAA T-2
levels and glutamate clearance that were further reduced by METH.aken T together, our data show that METH
treatment activated TAAR1 leading to intracellular cAMP in human astrocytes and modulated glutamate clearance
abilities. Furthermore, molecular alterations in astrocyte A
TAR1 levels correspond to changes in astrocyte EAA
T-2
levels and function."

Further reading
White, F.A.; Jung, H. & Miller, R.J. (2007). "Chemokines and the pathophysiology of neuropathic pain" . Proceedings
of the National Academy of Sciences of the United States of America . 104 (51): 20151–20158.
Bibcode:2007PNAS..10420151W. doi:10.1073/pnas.0709250104. PMC 2154400 . PMID 18083844.
Milligan, E.D. & Watson, L.R. (2009). "Pathological and protective roles of glia in chronic pain" . Neuron-Glia
Interactions. 10 (1): 23–36. doi:10.1038/nrn2533. PMC 2752436 . PMID 19096368.
Watkins, L.R.; Milligan, E.D. & Maier, S.F. (2001). "Glial activation: a driving force for pathological pain".Trends
Neurosci. 24 (8): 450–455. doi:10.1016/S0166-2236(00)01854-3. PMID 11476884.
Freeman, M. R. (2010)."Specification and Morphogenesis of Astrocytes" . Science. 330 (6005): 774–8.
Bibcode:2010Sci...330..774F. doi:10.1126/science.1190928. PMC 5201129 . PMID 21051628.
Verkhratsky, A.; Butt, A.M. (2013). "Numbers: how many glial cells are in the brain?". Glial Physiology and
Pathophysiology. John Wiley and Sons. pp. 93–96.ISBN 978-0-470-97853-5.

External links
Cell Centered Database – Astrocyte
UIUC Histology Subject57
"Astrocytes" at Society for Neuroscience
The Department of Neuroscienceat Wikiversity
NIF Search – Astrocytevia the Neuroscience Information Framework

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