Skip to content
naulon
Get started

No retraction, correction or concern found when last checked on Oct 21, 2026.

The multifaceted role of astrocytes in regulating myelination

Hülya Kıray, Susan L. Lindsay, Sara Hosseinzadeh and 1 more

Experimental Neurology · 2016 · Review · CC BY

doi:10.1016/j.expneurol.2016.03.009

Abstract

Astrocytes are the major glial cell of the central nervous system (CNS), providing both metabolic and physical support to other neural cells. After injury, astrocytes become reactive and express a continuum of phenotypes which may be supportive or inhibitory to CNS repair. This review will focus on the ability of astrocytes to influence myelination in the context of specific secreted factors, cytokines and other neural cell targets within the CNS. In particular, we focus on how astrocytes provide energy and cholesterol to neurons, influence synaptogenesis, affect oligodendrocyte biology and instigate cross-talk between the many cellular components of the CNS.

Full text

From PubMed Central, U.S. National Library of Medicine, as current on Oct 21, 2026. Paragraph numbers are ours, so an answer can point at one.

Introduction

Astrocytes were long considered secondary to neurons in central nervous system (CNS) function, and erroneously dismissed as “brain glue” (glia is the Greek term for glue). Research over the past two decades, however, has shown astrocytic roles extending to a range of brain functions far beyond basic physical and metabolic neuronal support. Astrocytic regulation of myelination was first hypothesised by Műller in 1904, who claimed that the demyelinating disease, Multiple Sclerosis (MS), was rooted in astrocytic dysfunction. Evidence has since continued to grow supporting the premise that astrocytes could be important in regulating myelination.

Glial fibrillary acidic protein (GFAP) has been used extensively in the study of astrocytes. Increased GFAP expression has been associated with astrocyte reactivity in CNS lesions and is a pathological hallmark of disease and/or injury. Fig. 1 illustrates astrocytes immunolabelled with GFAP and nestin, another marker thought to label reactive astrocytes. In experimental allergic encephalomyelitis (EAE), a widely used animal model of MS, where demyelination is induced by myelin antigens, administered together with adjuvant that contains bacterial components, GFAP expression was seen on more numerous and much larger astrocytic processes in chronic lesions compared to normal appearing white matter. Thus, the degree of GFAP immunoreactivity appears to reflect the level of reactive astrogliosis. This was reviewed in detail by, who described a continuum of phenotypic changes, that range from mild to severe, the latter resulting in glial scar formation. Attempts have also been made to define the astrocyte phenotype in more detail along this continuum. It has been suggested that mild astrogliosis is associated with astrocyte “activation” and severe astrogliosis is associated with “reactivity”, with the former promoting recovery of CNS function after injury and the latter walling off the injured area and preventing repair. Although activated astrocytes have been associated with less detrimental effects on the CNS and reactive astrocytes as more damaging, it is clear that these properties are not all or nothing and reactive astrocytes can also be beneficial to CNS repair. Interestingly, in studies using GFAP null mice, it was seen that animals had abnormal myelination, non-myelinated axons in the optic nerve with an age related reduction in myelin thickness. Non-conservative mutations in the GFAP gene have also been linked to the white matter brain disorder, Alexander disease. Therefore, the evidence for direct or indirect astrocytic roles on re/myelination has been established both by in vitro and in vivo studies.

Considering the limitations in the current treatments for demyelinating CNS diseases and injuries, it is crucial to identify other approaches to regulate myelination in search of novel strategies for repair. Astrocytes have been shown to promote myelination through their supportive roles on neuron survival and maintenance of neuronal activity, and their direct action on proliferation, differentiation and migration of oligodendrocytes (Fig. 2). This review will focus on the interaction of astrocytes with neural cells to synergistically promote myelination.

Role of cytokines and chemokines

It is apparent that astrocytes can affect myelination under a range of normal and pathological conditions, but it is important to understand how this is regulated. Many molecules can trigger or even regulate astrogliosis, including large polypeptide growth factors and cytokines, mediators of innate immunity such as lipopolysaccharide (LPS) and other Toll-like receptor ligands, neurotransmitters, purines, reactive oxygen species, and molecules related to hypoxia and glucose deprivation. For the purpose of this review we will focus on cytokines and chemokines. Although these compounds are primarily considered in the context of chemotaxis in immune cells, here we will highlight their roles on astrocyte activation and reactivity. These molecules can be produced in an autocrine or paracrine fashion by various cell types in the CNS including neurons, oligodendrocyte lineage cells, microglia, pericytes and endothelial cells. Not only do these factors influence astrocyte phenotype but they also can affect a range of neural and immune cell types.

Astrocyte activation (mild astrogliosis): a pro-reparative phenotype?

Astrocytes can be activated directly or indirectly. For example, in response to injury, microglia become activated and release the cytokine interleukin 1β (IL-1β, ), which is an early injury signal. The delay of astrocyte activation in mice lacking IL-1β, as well as in mice lacking IL-1 type 1 receptor suggests that microglial activation is necessary for astrocyte activation. It has also been suggested that ciliary neurotrophic factor (CNTF; a member of the IL-6 family of cytokines)treated astrocytes in vitro had a phenotype that was more supportive of CNS repair and thus are, by definition, activated. Under CNTF treatment, astrocytes upregulate expression of classical reactivity markers such as GFAP, vimentin, and clusterin, show cellular and nuclear hypertrophy, and increase their proliferation rate. There is a growing body of evidence for the promotion of neuronal survival by cytokine-activated astrocytes, potentially through secretion of various neurotrophic growth factors in the vicinity of neurons including nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), activity dependent neurotrophic factor (ADNF), hepatocyte growth factor (HGF), leukaemia inhibitory factor (LIF), fibroblast growth factor-2 (FGF-2) and CNTF (,,,,,; Fig. 3). Moreover, cultured spinal cord astrocytes, treated with CNTF, support the survival of a significantly greater number of ventral spinal motor neurons and promote neurite outgrowth better than unstimulated astrocytes. Other researchers have shown that cytokine-activated astrocytes can promote neurogenesis, possibly by stimulating the differentiation of neural stem cells (NSCs) residing in the subventricular zone and the dentate gyrus in adult animals. Because these multipotent NSCs can migrate beyond their sites of origin and can later differentiate into oligodendrocytes, neurons and microglia, they have the potential to enhance recovery from CNS injury and disease.

Importantly, activated astrocytes have also shown positive effects on myelination. Our own investigations have shown that CNTF activated astrocytes can promote the percentage of myelinated fibres in CNS rat cultures. Further evidence of this has been shown in mice infected with the A-59 strain of the mouse hepatitis virus (MHV-A59), an animal model for MS. These animals have been shown to secrete increased levels of CNTF during the remyelination phase and CNTF mRNA is induced in the remyelinating regions in cells exhibiting astrocytic features. It is suggested that the increase in IL-1β levels at early stages of CNS pathology stimulates the induction of CNTF mRNA and protein in astrocytes, a phenomenon which appears to be important for remyelination. This could be due to FGF-2 signalling as CNTF treatment elevates astrocytic levels of Fgf-2 mRNA significantly, whereas, IL-1 β shows no effect. Since FGF-2 can enhance OPC proliferation, it may produce more OPCs for subsequent myelination. Moreover, if the gp130 receptor, the ubiquitous signal transducer for CNTF and all IL-6 family members, is genetically removed from astrocytes, astrocyte survival was poor, there was a reduction in the development of astrogliosis, and larger areas of demyelination formed with a greater pro-inflammatory T cell response.

Therefore, CNTF seems to be an important cytokine involved in astrocyte reactivity and myelination. Interestingly, IL-1β can also stimulate the astrocytic production of another IL-6 family cytokine, LIF,, which has been shown to promote survival and differentiation of oligodendrocytes. LIF also decreases disease severity when exogenously administered in both chronic and relapsing-remitting EAE mice. Positive effects of LIF on the survival and maturation of oligodendrocytes also provides evidence for the positive roles of LIF on myelination. However, other pro-inflammatory cytokines such as tumour necrosis factor-alpha (TNF-α) and interferon-gamma (IFN-γ) have also been shown to potentiate reactive astrogliosis as discussed below.

Astrocyte reactivity (severe astrogliosis): an inhibitory phenotype?

In contrast to their positive effects on myelination, astrocytes can also have a more detrimental effect on CNS repair via the secretion of chemokines/cytokines when in a more severe, reactive state (Fig. 3). One such cytokine is TNF-α, which has been shown to induce myelin and oligodendrocyte damage in vitro. TNF-α mRNA expression in MS plaques positively correlates with the extent of demyelination and has been shown to be present in microglia/macrophages and to a smaller percentage of astrocytes. On the other hand, studies have shown TNF-α expression is mainly associated with GFAP positive fibrous astrocytes in chronic active MS lesions at the lesion edge as well as foamy macrophages and endothelial cells. However, the fact that astrocytes appear as the major or minor TNF-α expressing cell types in MS lesions might be because astrocytes internalize the protein in a receptor-mediated manner rather than producing it themselves as suggested by and. Moreover, it is possible that astrocytes require a longer period of time to become reactive upon injury and only produce TNF-α first at the lesion edge of acute MS plaques and later both at the lesion edge and in the lesion centre of chronic active plaques. In situ hybridisation for TNF-α mRNA has been detected in GFAP-positive astrocytes in mice suffering from pneumococcal meningitis which also suggests that astrocytes can indeed produce TNF-α in CNS pathologies.

Since TNF-α effects the maturation of oligodendrocytes, remyelination failure in the CNS lesions could be because TNF-α prevents the in situ differentiation of oligodendrocytes. Interestingly, direct cell contact between pre-oligodendrocytes (preOLs) and astrocytes has been shown to be a prerequisite for TNF to induce apoptosis in preOLs of rodent mixed glial cultures. Nevertheless, it is possible that TNF-α increases production of PDGF in demyelinated spinal cord lesions of MHV-A59-injected mice as suggested by the increase of PDGF-β transcription and PDGF-αβ protein levels in embryonic human astrocytes upon TNF-α treatment. Therefore, astrocytes might have a positive role on remyelination both by producing TNF-α and by secreting PDGF upon stimulation with TNF-α. PDGF could in turn support the survival and enhance the proliferation of OPCs in demyelinating lesions. Consequently, it is yet difficult to conclude whether reactive astrocytes associated with increased TNF-α levels in CNS lesions are predominantly stimulatory or inhibitory to remyelination.

IFN-γ, another cytokine found in MS plaques, has been reported to not only activate astrocytes, but is also expressed by reactive astrocytes and by immune cells that astrocytes have stimulated. Similar to TNF-α, IFN-γ has been shown to suppress remyelination and to delay disease recovery in transgenic EAE mice, where IFN-γ expression by astrocytes was stimulated temporally in the recovery stage. Astrocyte-directed expression of IFN-γ in transgenic mice has also resulted in regional hypomyelination and selective disruption of brain histogenesis, which led to ataxia and shorter life span. Furthermore, knocking down IFN-γ receptor expression in astrocytes three days before immunization suppressed EAE and demyelination by inhibiting inflammatory cell infiltration. These animals presented lower mean clinical scores even when the receptor silencing was initiated after disease onset or at disease peak. Despite the abovementioned evidence suggesting inhibitory roles for reactive astrocytes on myelination, have proposed that IFN-γ signalling in astrocytes is indispensable for the alleviation of EAE since levels of demyelination and axonal loss are increased during acute EAE in mice with an astrocytic expression of a dominant negative allele for IFN-γ receptor. Nevertheless, their approach blocked IFN-γ signalling in astrocytes without decreasing the expression of IFN-γ receptor, which would lower the levels of IFN-γ available for immunoregulatory cells; whereas, have knocked down the expression of the receptor itself. Therefore, blocking or lowering IFN-γ signalling in astrocytes with a carefully planned strategy might provide new disease-modifying treatments that will limit demyelination.

Reactive astrocytes also secrete C-X-C motif chemokine 10 (CXCL10, ), particularly around active MS lesions. Cxcl10 mRNA expression increases significantly during peak disease and decreases during the recovery phases in animal models of MS. A direct effect of CXCL10 on the inhibition of myelination was shown in dissociated rat spinal cord cells plated on astrocytes treated with CXCL10 and its neutralizing antibody. In these experiments CXCL10 identified by microarray analysis, was upregulated in an astrocyte phenotype that was inhibitory to CNS myelination in vitro. Specifically, CXCL10 appeared to inhibit oligodendrocyte process extension. Consequently, cytokines stand out as an important family of molecules to activate astrocytes and to initiate different forms of astrocyte reactivity that could be either beneficial or inhibitory for the CNS milieu in terms of re/myelination.

It should be noted that the secretion of such pro-inflammatory cytokines that can contribute to the lack of remyelination within MS plaques is not restricted to reactive astrocytes since other glial and inflammatory cell types will also secrete them. Moreover, the up regulation of such cytokines by reactive astrocytes can also be protective for CNS injury. For example, the astrocytic scar can restrict leukocyte migration from within areas of damaged tissue into the otherwise healthy non damaged CNS tissue in close proximity to the scar protecting it from immune mediated damage.

Astrocytes provide energy and cholesterol

A vital supportive role played by astrocytes following injury is the provision of an energy source, which is important if axons are to be myelinated. This energy is metabolized from glucose which enters the brain via the endothelial cells lining the blood brain barrier (BBB), which are in close contact with astrocytes. Unlike endothelial cells, astrocytes biochemically transform glucose into glycogen, the principal source of stored energy in all cell types. In addition, it has been suggested that astrocytes under low glucose concentrations can degrade stored glycogen into lactate which in turn increases extracellular lactate levels to provide energy for nearby axons when deprivation occurs after injury. The lactate derived from astroglial glycogen via glycolysis is transferred directly to the axon at the node of Ranvier. The importance of lactate during demyelination is only just emerging. Whether astrocytes maintain the energy levels of only axons as previously thought, or if this extends to oligodendrocytes as well, is an interesting concept. Oligodendrocytes are known to consume lactate at higher levels than other CNS cells, therefore making them an important user of any lactate production. Furthermore, promotion of myelination via oligodendrocytes has been shown when endogenous lactate is applied therefore at least some astrocytic lactate production may be targeted to myelinating oligodendrocytes. However, energy regulation in the CNS is more complex as recent evidence has shown that oligodendrocytes in turn can transfer glycolysis products such as lactate to axons via monocarboxylic acid transporters (MCT1, MCT2), which reside in internodal myelin and the axonal compartment.

Cholesterol is essential to every cell in the body as it is an important component of cellular membranes. In the CNS it is vital for normal brain development, is a precursor to many signalling molecules such as steroid hormones, and importantly, is a major structural component of myelin sheaths. The BBB prevents the transport of either hepatic or dietary cholesterol, meaning that cholesterol must be derived by de novo synthesis within the CNS. Astrocytes are proposed to be one of the primary cellular sources of cholesterol and mediate its secretion by their expression of several apolipoproteins, molecules that bind cholesterol. There is sufficient evidence to suggest that there is horizontal transfer of cholesterol with both astrocytes and oligodendrocytes producing cholesterol to maintain myelin sheath formation and neurons. This transfer between cells is critically relevant to neurodegenerative diseases, since the availability of cholesterol is thought to be an essential rate limiting factor to myelin production. Therefore, in addition to their roles in providing energy to neurons, astrocytes also emerge as important cholesterol-suppliers in the CNS, which is vital for myelination.

Astrocytes play a role in synaptic signal transmission and can modulate synapses

A further function of astrocytes is the removal of excitotoxic molecules from the extracellular space, thus supporting neuronal survival. They can actively remove excitotoxic glutamate and convert it to glutamine by increasing their levels of glutamate transporters and glutamine synthetase, thereby preventing neuronal cell death during brain pathology. Astrocytes can also release gliotransmitters such as glutamate, purine, GABA and D-serine into the synaptic cleft upon excitation by changes in neuronal synaptic activity and can thereby regulate neuronal excitability. Neurotransmitter released from the neuronal synapse can reach adjacent astrocytes, stimulating increases in intracellular Ca2 + concentrations, which then leads to the secretion of gliotransmitters. These regulatory molecules then can feedback to presynaptic nerve terminals to modulate synaptic neurotransmission. These observations have even given rise to the currently accepted ‘tripartite synapse’ hypothesis, where astrocytes form an active, integral regulatory component of the synapse. Recently, electron microscopy has also shown microglia interacting with neuronal synapses and playing a role in synapse maturation, synaptic remodelling, and synaptic activity. Evidence has shown that microglia secrete immune factors that play an important role in synaptic connections and illustrates the complexity of cross-talk between neural cells and the immune system. These researchers have suggested a change in name from tripartite synapse to the quad-partite synapse.

In addition to playing a role in synaptic signal transmission, astrocytes can also modulate synapses. It has been demonstrated that astrocytes secrete molecules such as thrombospondins that might be required for the formation, function and pruning of developing synapses. Both presynaptic and postsynaptic activity in purified rat retinal ganglion cultures have been enhanced in the presence of astrocytes; and immunohistochemistry of rat brain cryosections from various developmental stages have shown that glial generation precedes the appearance of synapses. Astrocytes might also be functional in synaptic remodelling and pruning in healthy or diseased adult CNS. Because synaptic signal transmission can trigger astrocytes to secrete the cytokine LIF, which in turn increases the number of myelinated axons in dorsal root ganglion cultures co-cultured with oligodendrocytes, the support and maintenance of healthy signal transmission appears important for the regulation of myelination.

Furthermore, astrocytes may contribute to synaptic transmission by supporting maintenance of the synaptic interstitial fluid by regulating ion, pH and transmitter homeostasis. Astrocyte processes contain transporters for potassium uptake and aquaporin 4 water channels, which maintain the transmitter homeostasis of the synaptic interstitial fluid. Connexin channels and connexin proteins are important candidates which play a role in the regulation of neuronal activity and survival. For example, astroglial connexins decrease neuronal excitability by removing extracellular potassium and glutamate; while also providing metabolic supply to neurons. On the other hand, the elevation of connexin expression at lesion sites in CNS pathologies might also be associated with other, possibly protective, roles. Studies using connexin knockout animals allude to the importance of connexins in promoting communication between astrocytes and between astrocytes and oligodendrocytes on myelin integrity. Myelin damage has been observed in Cx47, Cx43/Cx30 and Cx30/Cx47 single/double knockout mice. Interestingly, the level of oligodendrocyte gap junction connexins Cx47 and Cx32 were reduced both within and around lesions during early stages of inflammatory demyelination in EAE mice,. These mice also presented decreased expression of Cx43, the major astrocytic partner of Cx47, when spinal cord sections were analysed immunohistochemically. Cx43 expression was increased at late EAE stages, where remyelination was observed, leading to the suggestion that astrocytic protein Cx43 might play an important role in recovery from neuroinflammation.

Astrocytic effects on oligodendrocyte precursor cell (OPC) survival, proliferation and maturation

In the 1980s advancements were made on the ability to grow purified cultures of glial cells, with Raff and colleagues in particular developing techniques to purify OPCs from the optic nerve, a tissue devoid of neuronal cell bodies. With the development of these culture techniques it was shown that astrocytes play important roles in OPC differentiation and in the rate of oligodendrocyte axonal ensheathment. Further in vitro studies, where conditioned medium collected from primary astrocyte monolayers was incubated with other neural cells, showed enhanced neuronal survival, proliferation of OPCs, and protection of oligodendrocytes from stress. It is likely that astrocytes support OPC survival and proliferation by providing soluble factors such as platelet derived growth factor (PDGF) and FGF-2.

Astrocytes are important providers of secreted growth factors, for both neuronal and glial proliferation and survival. For example, CNTF, although shown to be important in the activation of astrocytes, is constitutively expressed by white matter astrocytes, and is a key player in OPC survival and maturation in vitro and in vivo as discussed earlier. CNTF has also been reported to enhance the migration of subventricular zone-derived progenitors, protect oligodendrocytes from apoptosis, and decrease myelin destruction in demyelinating pathological conditions. In studies when CNTF was injected subcutaneously at the remyelination phase of cuprizone-induced demyelination, an increase was seen in myelin oligodendrocyte glycoprotein (MOG) expression in the cerebral cortex. Moreover, intraperitoneal injections of CNTF and intravenously transplanted mesenchymal stem cells that overexpress CNTF resulted in a reduced loss of neurons and disease severity, and increased neuronal functional recovery in EAE mice. However, in these experiments it is difficult to see if the effect is on the activation status of the astrocytes as discussed above, or the direct effect on the OPC.

Astrocytes have also been shown to exhibit a crucial role in OPC remyelination via their iron exporter ferroportin (Fpn) in mice, where focal demyelination was induced by the injection of lysophosphatidylcholine (LPC) into their spinal cords. In these astrocyte-specific Fpn KO mice, fewer remyelinating axons and a reduction in OPC proliferation were observed following LPC-induced demyelination compared to control animals. This could either be due to direct effects on OPCs through limited iron supply or indirect effects via iron-deficient microglia, which expressed significantly lower levels of TNF-α and IL-1β when stimulated by LPS compared to control microglia. Because the expression of FGF-2 and insulin-like growth factor-1 (IGF-1) was significantly upregulated by IL-1β and TNF-α, respectively, and the expression of transforming growth factor beta (TGF-β) was stimulated by IL-1β in purified astrocyte cultures, it has been suggested that iron-deprivation in the milieu would lower the expression of IL-1β and TNF-α in microglia and thus lead to reduced growth factor expression in astrocytes, which would in turn render OPC proliferation and possibly differentiation.

Future directions in astrocyte research

As discussed throughout this review astrocytes can play important roles not just in myelination during development, but also in remyelination in adult tissue after CNS injury. Their reparative roles might be related to their level of reactivity, so it is important to identify markers that can define these different astrocyte phenotypes although at present these are not easy to define. One approach is to use microarrays. As described, identified CXCL10 as inhibitory to myelination, but others using a lower-scale cDNA array that contained probes for cytokines, chemokines, growth factors and their receptors have identified other pro-inflammatory cytokines including TNF-α, IL-1β, or IFN-γ. Another large array was carried out on GFP-astrocytes purified at various time points after the onset of two models of disease, namely ischemic stroke (middle cerebral artery occlusion) and neuroinflammation induced by LPS injection. The resulting data suggested that astrocytes could present different mRNA expression profiles depending on the insult despite the presence of reactive gliosis in both types of CNS damage. However, although there was upregulation of a core set of genes (lipocalin 2 and serpina3n), it was clear that changes in the astrocyte after injury are highly heterogeneous, and that changes in astrocyte activity may depend on the injury type. Hopefully, more specific markers of “good” or “bad” astrocytes for CNS repair will be identified and allow more specific identification of how these astrocytes influence repair.

Summary and conclusions

There is abundant evidence to suggest that astrocytes contribute to re/myelination mainly by:

1) Providing the right conditions for neurons to myelinate by i) supplying neurons with energy and cholesterol, ii) removing excitotoxic molecules from the extracellular environment, and iii) regulating the fluid, ion, pH, and neuro/gliotransmitter homeostasis.

2) Playing a role in the survival, proliferation, maturation and function of oligodendrocytes and the migration of OPCs into the lesioned areas in the CNS.

3) Influencing microglia.

The manner by which astrocytes affect myelination can often be seen to correlate with its level of reactivity. Astrocyte reactivity can be induced by the milieu of cytokines present after injury, which can be beneficial or inhibitory in re/myelination depending on the context and severity of the injury. Due to the lack of gliosis-specific markers, there are currently no clear guidelines which allow different astrocytic reactivity phenotypes to be classified. However, if markers can be identified that classify the continuum of astrocyte phenotypes, it may aid in the design of new treatments targeting phenotypes that are more suited to regeneration and remyelination, and therefore benefit in the treatment of demyelinating diseases.

References 160

  1. 1.

    Albrecht P.J., Dahl J.P., Stoltzfus O.K., Levenson R., Levison S.W. Ciliary neurotrophic factor activates spinal cord astrocytes, stimulating their production and release of fibroblast growth factor-2, to increase motor neuron survival. Exp. Neurol. 2002;173:46-62.

    Not in our library10.1006/exnr.2001.7834

  2. 2.

    Albrecht P.J., Murtie J.C., Ness J.K., Redwine J.M., Enterline J.R., Armstrong R.C., Levison S.W. Astrocytes produce CNTF during the remyelination phase of viral-induced spinal cord demyelination to stimulate FGF-2 production. Neurobiol. Dis. 2003;13:89-101.

    Not in our library10.1016/s0969-9961(03)00019-6

  3. 3.

    Albrecht P.J., Enterline J.C., Cromer J., Levison S.W. CNTF-activated astrocytes release a soluble trophic activity for oligodendrocyte progenitors. Neurochem. Res. 2007;32:263-271.

    Not in our library10.1007/s11064-006-9151-6

  4. 4.

    Aloisi F., Rosa S., Testa U., Bonsi P., Russo G., Peschle C., Levi G. Regulation of leukemia inhibitory factor synthesis in cultured human astrocytes. J. Immunol. 1994;152:5022-5031.

    Not in our library

  5. 5.

    Amiry-Moghaddam M., Williamson A., Palomba M., Eid T., de Lanerolle N.C., Nagelhus E.A., Adams M.E., Froehner S.C., Agre P., Ottersen O.P. Delayed K + clearance associated with aquaporin-4 mislocalization: phenotypic defects in brains of alpha-syntrophin-null mice. Proc. Natl. Acad. Sci. 2003;100:13615-13620.

    Not in our library10.1073/pnas.2336064100

  6. 6.

    Arai K., Lo E.H. Astrocytes protect oligodendrocyte precursor cells via MEK/ERK and PI3K/Akt signaling. J. Neurosci. Res. 2010;88:758-763.

    Not in our library10.1002/jnr.22256

  7. 7.

    Araque A., Parpura V., Sanzgiri R.P., Haydon P.G. Glutamate-dependent astrocyte modulation of synaptic transmission between cultured hippocampal neurons. Eur. J. Neurosci. 1998;10:2129-2142.

    Not in our library10.1046/j.1460-9568.1998.00221.x

  8. 8.

    Araque A., Parpura V., Sanzgiri R.P., Haydon P.G. Tripartite synapses: glia, the unacknowledged partner. Trends Neurosci. 1999;22:208-215.

    Not in our library10.1016/s0166-2236(98)01349-6

  9. 9.

    Aránguez I., Torres C., Rubio N. The receptor for tumor necrosis factor on murine astrocytes: characterization, intracellular degradation, and regulation by cytokines and Theiler's murine encephalomyelitis virus. Glia. 1995;13:185-194.

    Not in our library10.1002/glia.440130305

  10. 10.

    Auron P.E. The interleukin 1 receptor: ligand interactions and signal transduction. Cyto. Growth Factor Rev. 1998;9:221-237.

    Not in our library10.1016/s1359-6101(98)00018-5

  11. 11.

    Barnett S.C., Linington C. Myelination: do astrocytes play a role? Neuroscientist. 2013;19:442-450.

    Not in our library10.1177/1073858412465655

  12. 12.

    Barres B.A. The mystery and magic of glia: a perspective on their roles in health and disease. Neuron. 2008;60:430-440.

    Not in our library10.1016/j.neuron.2008.10.013

  13. 13.

    Bekar L.K., He W., Nedergaard M. Locus coeruleus alpha-adrenergic-mediated activation of cortical astrocytes in vivo. Cereb. Cortex. 2008;18:2789-2795.

    Not in our library10.1093/cercor/bhn040

  14. 14.

    Bergles D.E., Jahr C.E. Synaptic activation of glutamate transporters in hippocampal astrocytes. Neuron. 1997;19:1297-1308.

    Not in our library10.1016/s0896-6273(00)80420-1

  15. 15.

    Bezzi P., Carmignoto G., Pasti L., Vesce S., Rossi D., Rizzini B.L., Pozzan T., Volterra A. Prostaglandins stimulate calcium-dependent glutamate release in astrocytes. Nature. 1998;391:281-285.

    Not in our library10.1038/34651

  16. 16.

    Bitsch A., Kuhlmann T., Da Costa C., Bunkowski S., Polak T., Brück W. Tumour necrosis factor alpha mRNA expression in early multiple sclerosis lesions: correlation with demyelinating activity and oligodendrocyte pathology. Glia. 2000;29:366-375.

    Not in our library10.1002/(sici)1098-1136(20000215)29:4<366::aid-glia7>3.0.co;2-y

  17. 17.

    Bögler O., Wren D., Barnett S.C., Land H., Noble M. Cooperation between two growth factors promotes extended self-renewal and inhibits differentiation of oligodendrocyte-type-2 astrocyte (O-2 A) progenitor cells. Proc. Natl. Acad. Sci. 1990;87:6368-6372.

    Not in our library10.1073/pnas.87.16.6368

  18. 18.

    Boyles J.K., Pitas R.E., Wilson E., Mahley R.W., Taylor J.M. Apolipoprotein E associated with astrocytic glia of the central nervous system and with nonmyelinating glia of the peripheral nervous system. J. Clin. Invest. 1985;76:1501-1513.

    Not in our library10.1172/jci112130

  19. 19.

    Brenner M., Johnson A.B., Boespflug-Tanguy O., Rodriguez D., Goldman J.E., Messing A. Mutations in GFAP, encoding glial fibrillary acidic protein, are associated with Alexander disease. Nat. Genet. 2001;27:117-120.

    Not in our library10.1038/83679

  20. 20.

    Bugga L., Gadient R.A., Kwan K., Stewart C.L., Patterson P.H. Analysis of neuronal and glial phenotypes in brains of mice deficient in leukemia inhibitory factor. J. Neurobiol. 1998;36:509-524.

    Not in our library10.1002/(sici)1097-4695(19980915)36:4<509::aid-neu5>3.0.co;2-#

  21. 21.

    Butzkueven H., Zhang J.G., Soilu-Hanninen M., Hochrein H., Chionh F., Shipham K.A., Emery B., Turnley A.M., Petratos S., Ernst M., Bartlett P.F., Kilpatrick T.J. LIF receptor signaling limits immune-mediated demyelination by enhancing oligodendrocyte survival. Nat. Med. 2002;8:613-619.

    Not in our library10.1038/nm0602-613

  22. 22.

    Cammer W., Zhang H. Maturation of oligodendrocytes is more sensitive to TNF alpha than is survival of precursors and immature oligodendrocytes. J. Neuroimmunol. 1999;97:37-42.

    Not in our library10.1016/s0165-5728(99)00045-4

  23. 23.

    Cao Q., He Q., Wang Y., Cheng X., Howard R.M., Zhang Y., DeVries W.H., Shields C.B., Magnuson D.S., Xu X.M., Kim D.H., Whittemore S.R. Transplantation of ciliary neurotrophic factor-expressing adult oligodendrocyte precursor cells promotes remyelination and functional recovery after spinal cord injury. J. Neurosci. 2010;30:2989-3001.

    Not in our library10.1523/jneurosci.3174-09.2010

  24. 24.

    Carter S.L., Müller M., Manders P.M., Campbell I.L. Induction of the genes for Cxcl9 and Cxcl10 is dependent on IFN-gamma but shows differential cellular expression in experimental autoimmune encephalomyelitis and by astrocytes and microglia in vitro. Glia. 2007;55:1728-1739.

    Not in our library10.1002/glia.20587

  25. 25.

    Christopherson K.S., Ullian E.M., Stokes C.C., Mullowney C.E., Hell J.W., Agah A., Lawler J., Mosher D.F., Bornstein P., Barres B.A. Thrombospondins are astrocyte-secreted proteins that promote CNS synaptogenesis. Cell. 2005;120:421-433.

    Not in our library10.1016/j.cell.2004.12.020

  26. 26.

    Coco S., Calegari F., Pravettoni E., Pozzi D., Taverna E., Rosa P., Matteoli M., Verderio C. Storage and release of ATP from astrocytes in culture. J. Biol. Chem. 2003;278:1354-1362.

    Not in our library10.1074/jbc.m209454200

  27. 27.

    Dallner C., Woods A.G., Deller T., Kirsch M., Hofmann H.D. CNTF and CNTF receptor alpha are constitutively expressed by astrocytes in the mouse brain. Glia. 2002;37:374-378.

    Not in our library

  28. 28.

    Ding X., Yan Y., Li X., Li K., Ciric B., Yang J., Zhang Y., Wu S., Xu H., Chen W., Lovett-Racke A.E., Zhang G.X., Rostami A. Silencing IFN-γ binding/signaling in astrocytes versus microglia leads to opposite effects on central nervous system autoimmunity. J. Immunol. 2015;194:4251-4264.

    Not in our library10.4049/jimmunol.1303321

  29. 29.

    Dreyfus C.F., Dai X., Lercher L.D., Racey B.R., Friedman W.J., Black I.B. Expression of neurotrophins in the adult spinal cord in vivo. J. Neurosci. Res. 1999;56:1-7.

    Not in our library10.1002/(sici)1097-4547(19990401)56:1<1::aid-jnr1>3.0.co;2-3

  30. 30.

    Eng L.F., Vanderhaeghen J.J., Bignami A., Gerstl B. An acidic protein isolated from fibrous astrocytes. Brain Res. 1971;28:351-354.

    Not in our library10.1016/0006-8993(71)90668-8

  31. 31.

    Eng D.L., Lee Y.L., Lal P.G. Expression of glutamate uptake transporters after dibutyryl cyclic AMP differentiation and traumatic injury in cultured astrocytes. Brain Res. 1997;778:215-221.

    Not in our library10.1016/s0006-8993(97)01093-7

  32. 32.

    Faden A.I., Demediuk P., Panter S.S., Vink R. The role of excitatory amino acids and NMDA receptors in traumatic brain injury. Science. 1989;244:798-800.

    Not in our library10.1126/science.2567056

  33. 33.

    Farina C., Aloisi F., Meinl E. Astrocytes are active players in cerebral innate immunity. Trends Immunol. 2007;28:138-145.

    Not in our library10.1016/j.it.2007.01.005

  34. 34.

    Faulkner J.R., Herrmann J.E., Woo M.J., Tansey K.E., Doan N.B., Sofroniew M.V. Reactive astrocytes protect tissue and preserve function after spinal cord injury. J. Neurosci. 2004;24:2143-2155.

    Not in our library10.1523/jneurosci.3547-03.2004

  35. 35.

    Ferrara N., Ousley F., Gospodarowicz D. Bovine brain astrocytes express basic fibroblast growth factor, a neurotropic and angiogenic mitogen. Brain Res. 1988;462:223-232.

    Not in our library10.1016/0006-8993(88)90550-1

  36. 36.

    Fife B.T., Kennedy K.J., Paniagua M.C., Lukacs N.W., Kunkel S.L., Luster A.D., Karpus W.J. CXCL10 (IFN-gamma-inducible protein-10) control of encephalitogenic CD4 + T cell accumulation in the central nervous system during experimental autoimmune encephalomyelitis. J. Immunol. 2001;166:7617-7624.

    Not in our library10.4049/jimmunol.166.12.7617

  37. 37.

    Froger N., Orellana J.A., Calvo C.F., Amigou E., Kozoriz M.G., Naus C.C., Sáez J.C., Giaume C. Inhibition of cytokine-induced connexin43 hemichannel activity in astrocytes is neuroprotective. Mol. Cell. Neurosci. 2010;45:37-46.

    Not in our library10.1016/j.mcn.2010.05.007

  38. 38.

    Frost E.E., Nielsen J.A., Le T.Q., Armstrong R.C. PDGF and FGF2 regulate oligodendrocyte progenitor responses to demyelination. J. Neurobiol. 2003;54:457-472.

    Not in our library10.1002/neu.10158

  39. 39.

    Fujita H., Sato K., Wen T.C., Peng Y., Sakanaka M. Differential expressions of glycine transporter 1 and three glutamate transporter mRNA in the hippocampus of gerbils with transient forebrain ischemia. J. Cereb. Blood Flow Metab. 1999;19:604-615.

    Not in our library10.1097/00004647-199906000-00003

  40. 40.

    Fünfschilling U., Supplie L.M., Mahad D., Boretius S., Saab A.S., Edgar J., Brinkmann B.G., Kassmann C.M., Tzvetanova I.D., Möbius W., Diaz F., Meijer D., Suter U., Hamprecht B., Sereda M.W., Moraes C.T., Frahm J., Goebbels S., Nave K.A. Glycolytic oligodendrocytes maintain myelin and long-term axonal integrity. Nature. 2012;485:517-521.

    Not in our library10.1038/nature11007

  41. 41.

    Glabinski A.R., Tani M., Strieter R.M., Tuohy V.K., Ransohoff R.M. Synchronous synthesis of alpha- and beta-chemokines by cells of diverse lineage in the central nervous system of mice with relapses of chronic experimental autoimmune encephalomyelitis. Am. J. Pathol. 1997;150:617-630.

    Not in our library

  42. 42.

    Godiska R., Chantry D., Dietsch G.N., Gray P.W. Chemokine expression in murine experimental allergic encephalomyelitis. J. Neuroimmunol. 1995;58:167-176.

    Not in our library10.1016/0165-5728(95)00008-p

  43. 43.

    Gundersen V., Ottersen O.P., Storm-Mathisen J. Selective excitatory amino acid uptake in glutamatergic nerve terminals and in glia in the rat striatum: quantitative electron microscopic immunocytochemistry of exogenous (D)-aspartate and endogenous glutamate and GABA. Eur. J. Neurosci. 1996;8:758-765.

    Not in our library10.1111/j.1460-9568.1996.tb01261.x

  44. 44.

    Guthrie K.M., Woods A.G., Nguyen T., Gall C.M. Astroglial ciliary neurotrophic factor mRNA expression is increased in fields of axonal sprouting in deafferented hippocampus. J. Comp. Neurol. 1997;386:137-148.

    Not in our library

  45. 45.

    Halassa M.M., Fellin T., Haydon P.G. The tripartite synapse: roles for gliotransmission in health and disease. Trends Mol. Med. 2007;13:54-63.

    Not in our library10.1016/j.molmed.2006.12.005

  46. 46.

    Haroon F., Drögemüller K., Händel U., Brunn A., Reinhold D., Nishanth G., Mueller W., Trautwein C., Ernst M., Deckert M., Schlűter D. Gp130-dependent astrocytic survival is critical for the control of autoimmune central nervous system inflammation. J. Immunol. 2011;186:6521-6531.

    Not in our library10.4049/jimmunol.1001135

  47. 47.

    Hashioka S., Klegeris A., Schwab C., Mcgeer P.L. Interferon-gamma-dependent cytotoxic activation of human astrocytes and astrocytoma cells. Neurobiol. Aging. 2009;30:1924-1935.

    Not in our library10.1016/j.neurobiolaging.2008.02.019

  48. 48.

    Herrmann J.E., Imura T., Song B., Qi J., Ao Y., Nguyen T.K., Korsak R.A., Takeda K., Akira S., Sofroniew M.V. STAT3 is a critical regulator of astrogliosis and scar formation after spinal cord injury. J. Neurosci. 2008;28:7231-7243.

    Not in our library10.1523/jneurosci.1709-08.2008

  49. 49.

    Herx L.M., Rivest S., Yong V.W. Central nervous system-initiated inflammation and neurotrophism in trauma: IL-1 beta is required for the production of ciliary neurotrophic factor. J. Immunol. 2000;165:2232-2239.

    Not in our library10.4049/jimmunol.165.4.2232

  50. 50.

    Hindinger C., Bergmann C.C., Hinton D.R., Phares T.W., Parra G.I., Hussain S., Savarin C., Atkinson R.D., Stohlman S.A. IFN-γ signaling to astrocytes protects from autoimmune mediated neurological disability. PLoS ONE. 2012;7.

    Not in our library10.1371/journal.pone.0042088

  51. 51.

    Hirrlinger J., Nave K.A. Adapting brain metabolism to myelination and long-range signal transduction. Glia. 2014;62:1749-1761.

    Not in our library10.1002/glia.22737

  52. 52.

    Hofman F.M., Hinton D.R., Johnson K., Merrill J.E. Tumor necrosis factor identified in multiple sclerosis brain. J Exp. Med. 1989;170:607-612.

    Not in our library10.1084/jem.170.2.607

  53. 53.

    Hudgins S.N., Levison S.W. Ciliary neurotrophic factor stimulates astroglial hypertrophy in vivo and in vitro. Exp. Neurol. 1998;150:171-182.

    Not in our library10.1006/exnr.1997.6735

  54. 54.

    Ionescu V.A., Villanueva E.B., Hashioka S., Bahniwal M., Klegeris A. Cultured adult porcine astrocytes and microglia express functional interferon-γ receptors and exhibit toxicity towards SH-SY5Y cells. Brain Res. Bull. 2011;84:244-251.

    Not in our library10.1016/j.brainresbull.2010.12.011

  55. 55.

    Ishibashi T., Dakin K.A., Stevens B., Lee P.R., Kozlov S.V., Stewart C.L., Fields R.D. Astrocytes promote myelination in response to electrical impulses. Neuron. 2006;49:823-832.

    Not in our library10.1016/j.neuron.2006.02.006

  56. 56.

    Izadpanah K., Freyer D., Weber J.R., Braun J.S. Brain parenchymal TNF-α and IL-1β induction in experimental pneumococcal meningitis. J. Neuroimmunol. 2014;276:104-111.

    Not in our library10.1016/j.jneuroim.2014.08.625

  57. 57.

    Ji K., Miyauchi J., Tsirka S.E. Microglia: an active player in the regulation of synaptic activity. Neural. Plast. 2013;2013:627325.

    Not in our library10.1155/2013/627325

  58. 58.

    John G.R., Lee S.C., Brosnan C.F. Cytokines: powerful regulators of glial cell activation. Neuroscientist. 2003;9:10-22.

    Not in our library10.1177/1073858402239587

  59. 59.

    Jordan C.A., Friedrich V.L., Godfraind C., Cardellechio C.B., Holmes K.V., Dubois-Dalcq M. Expression of viral and myelin gene transcripts in a murine CNS demyelinating disease caused by a coronavirus. Glia. 1989;2:318-329.

    Not in our library10.1002/glia.440020505

  60. 60.
    GFAP Isoforms in Adult Mouse Brain with a Focus on Neurogenic Astrocytes and Reactive Astrogliosis in Mouse Models of Alzheimer Disease · 2012
    No notice
  61. 61.

    Karpuk N., Burkovetskaya M., Fritz T., Angle A., Kielian T. Neuroinflammation leads to region-dependent alterations in astrocyte gap junction communication and hemichannel activity. J. Neurosci. 2011;31:414-425.

    Not in our library10.1523/jneurosci.5247-10.2011

  62. 62.

    Khan M.A., De Vellis J. Regulation of an oligodendrocyte progenitor cell line by the interleukin-6 family of cytokines. Glia. 1994;12:87-98.

    Not in our library10.1002/glia.440120202

  63. 63.

    Kim S., Steelman A.J., Koito H., Li J. Astrocytes promote TNF-mediated toxicity to oligodendrocyte precursors. J. Neurochem. 2011;116:53-66.

    Not in our library10.1111/j.1471-4159.2010.07084.x

  64. 64.

    Koulakoff A., Ezan P., Giaume C. Neurons control the expression of connexin 30 and connexin 43 in mouse cortical astrocytes. Glia. 2008;56:1299-1311.

    Not in our library10.1002/glia.20698

  65. 65.

    Krum J.M., Phillips T.M., Rosenstein J.M. Changes in astroglial GLT-1 expression after neural transplantation or stab wounds. Exp. Neurol. 2002;174:137-149.

    Not in our library10.1006/exnr.2002.7867

  66. 66.

    Kuchibhotla K.V., Lattarulo C.R., Hyman B.T., Bacskai B.J. Synchronous hyperactivity and intercellular calcium waves in astrocytes in Alzheimer mice. Science. 2009;323:1211-1215.

    Not in our library10.1126/science.1169096

  67. 67.

    Kuhlmann T., Remington L., Cognet I., Bourbonniere L., Zehntner S., Guilhot F., Herman A., Guay-Giroux A., Antel J.P., Owens T., Gauchat J.F. Continued administration of ciliary neurotrophic factor protects mice from inflammatory pathology in experimental autoimmune encephalomyelitis. Am. J. Pathol. 2006;169:584-598.

    Not in our library10.2353/ajpath.2006.051086

  68. 68.

    Kurumada S., Onishi A., Imai H., Ishii K., Kobayashi T., Sato S.B. Stage-specific association of apolipoprotein A-I and E in developing mouse retina. Invest. Ophthalmol. Vis. Sci. 2007;48:1815-1823.

    Not in our library10.1167/iovs.06-0902

  69. 69.

    Laferla F.M., Sugarman M.C., Lane T.E., Leissring M.A. Regional hypomyelination and dysplasia in transgenic mice with astrocyte-directed expression of interferon-gamma. J. Mol. Neurosci. 2000;15(1):45-59.

    Not in our library10.1385/jmn:15:1:45

  70. 70.

    Levison S.W., Ducceschi M.H., Young G.M., Wood T.L. Acute exposure to CNTF in vivo induces multiple components of reactive gliosis. Exp. Neurol. 1996;141:256-268.

    Not in our library10.1006/exnr.1996.0160

  71. 71.

    Levison S.W., Hudgins S.N., Crawford J.L. Ciliary neurotrophic factor stimulates nuclear hypertrophy and increases the GFAP content of cultured astrocytes. Brain Res. 1998;803:189-193.

    Not in our library10.1016/s0006-8993(98)00594-0

  72. 72.

    Li R., Messing A., Goldman J.E., Brenner M. GFAP mutations in Alexander disease. Int. J. Dev. Neurosci. 2002;20:259-268.

    Not in our library10.1016/s0736-5748(02)00019-9

  73. 73.

    Liberto C.M., Albrecht P.J., Herx L.M., Yong V.W., Levison S.W. Pro-regenerative properties of cytokine-activated astrocytes. J. Neurochem. 2004;89:1092-1100.

    Not in our library10.1111/j.1471-4159.2004.02420.x

  74. 74.

    Liedtke W., Edelmann W., Bieri P.L., Chiu F.C., Cowan N.J., Kucherlapati R., Raine C.S. GFAP is necessary for the integrity of CNS white matter architecture and long-term maintenance of myelination. Neuron. 1996;17:607-615.

    Not in our library10.1016/s0896-6273(00)80194-4

  75. 75.

    Lin C.T., Xu Y.F., Wu J.Y., Chan L. Immunoreactive apolipoprotein E is a widely distributed cellular protein. Immunohistochemical localization of apolipoprotein E in baboon tissues. J. Clin. Invest. 1986;78:947-958.

    Not in our library10.1172/jci112685

  76. 76.

    Lin W., Kemper A., Dupree J.L., Harding H.P., Ron D., Popko B. Interferon-gamma inhibits central nervous system remyelination through a process modulated by endoplasmic reticulum stress. Brain. 2006;129:1306-1318.

    Not in our library10.1093/brain/awl044

  77. 77.

    Linker R.A., Maurer M., Gaupp S., Martini R., Holtmann B., Giess R., Rieckmann P., Lassmann H., Toyka K.V., Sendtner M., Gold R. CNTF is a major protective factor in demyelinating CNS disease: a neurotrophic cytokine as modulator in neuroinflammation. Nat. Med. 2002;8:620-624.

    Not in our library10.1038/nm0602-620

  78. 78.

    Liu J.P., Tang Y., Zhou S., Toh B.H., Mclean C., Li H. Cholesterol involvement in the pathogenesis of neurodegenerative diseases. Mol. Cell. Neurosci. 2010;43:33-42.

    Not in our library10.1016/j.mcn.2009.07.013

  79. 79.

    Lu Z., Hu X., Zhu C., Wang D., Zheng X., Liu Q. Overexpression of CNTF in mesenchymal stem cells reduces demyelination and induces clinical recovery in experimental autoimmune encephalomyelitis mice. J. Neuroimmunol. 2009;206:58-69.

    Not in our library10.1016/j.jneuroim.2008.10.014

  80. 80.

    Lutz S.E., Zhao Y., Gulinello M., Lee S.C., Raine C.S., Brosnan C.F. Deletion of astrocyte connexins 43 and 30 leads to a dysmyelinating phenotype and hippocampal CA1 vacuolation. J. Neurosci. 2009;29:7743-7752.

    Not in our library10.1523/jneurosci.0341-09.2009

  81. 81.

    Markoullis K., Sargiannidou I., Gardner C., Hadjisavvas A., Reynolds R., Kleopa K.A. Disruption of oligodendrocyte gap junctions in experimental autoimmune encephalomyelitis. Glia. 2012;60:1053-1066.

    Not in our library10.1002/glia.22334

  82. 82.

    May P., Rohlmann A., Bock H.H., Zurhove K., Marth J.D., Schomburg E.D., Noebels J.L., Beffert U., Sweatt J.D., Weeber E.J., Herz J. Neuronal LRP1 functionally associates with postsynaptic proteins and is required for normal motor function in mice. Mol. Cell. Biol. 2004;24:8872-8883.

    Not in our library10.1128/mcb.24.20.8872-8883.2004

  83. 83.

    Mayer M., Bhakoo K., Noble M. Ciliary neurotrophic factor and leukemia inhibitory factor promote the generation, maturation and survival of oligodendrocytes in vitro. Dev. 1994;120:143-153.

    Not in our library10.1242/dev.120.1.143

  84. 84.

    Meeuwsen S., Persoon-Deen C., Bsibsi M., Ravid R., Van Noort J.M. Cytokine, chemokine and growth factor gene profiling of cultured human astrocytes after exposure to proinflammatory stimuli. Glia. 2003;43:243-253.

    Not in our library10.1002/glia.10259

  85. 85.

    Mei X., Ezan P., Giaume C., Koulakoff A. Astroglial connexin immunoreactivity is specifically altered at β-amyloid plaques in β-amyloid precursor protein/presenilin1 mice. Neuroscience. 2010;171:92-105.

    Not in our library10.1016/j.neuroscience.2010.08.001

  86. 86.

    Menichella D.M., Goodenough D.A., Sirkowski E., Scherer S.S., Paul D.L. Connexins are critical for normal myelination in the CNS. J. Neurosci. 2003;23:5963-5973.

    Not in our library10.1523/jneurosci.23-13-05963.2003

  87. 87.

    Mennerick S., Benz A., Zorumski C.F. Components of glial responses to exogenous and synaptic glutamate in rat hippocampal microcultures. J. Neurosci. 1996;16:55-64.

    Not in our library10.1523/jneurosci.16-01-00055.1996

  88. 88.

    Messersmith D.J., Murtie J.C., Le T.Q., Frost E.E., Armstrong R.C. Fibroblast growth factor 2 (FGF2) and FGF receptor expression in an experimental demyelinating disease with extensive remyelination. J. Neurosci. Res. 2000;62:241-256.

    Not in our library10.1002/1097-4547(20001015)62:2<241::aid-jnr9>3.0.co;2-d

  89. 89.

    Miljkovic D., Momcilovic M., Stojanovic I., Stosic-grujicic S., Ramic Z., Mostarica-stojkovic M. Astrocytes stimulate interleukin-17 and interferon-gamma production in vitro. J. Neurosci. Res. 2007;85:3598-3606.

    Not in our library10.1002/jnr.21453

  90. 90.

    Moore C.S., Abdullah S.L., Brown A., Areulpragasam A., Crocker S.J. How factors secreted from astrocytes impact myelin repair. J. Neurosci. Res. 2011;89:13-21.

    Not in our library10.1002/jnr.22482

  91. 91.
    d-Serine is an endogenous ligand for the glycine site of the N-methyl-d-aspartate receptor · 2000
    Not checked
  92. 92.

    Müller E., Fisher G. Pathologische anatomie und pathogenese. Die multiple Skleroze des Gehirns und Rückenmarks: Jena. 1904;300-344.

    Not in our library

  93. 93.

    Nagy J.I., Li W., Hertzberg E.L., Marotta C.A. Elevated connexin43 immunoreactivity at sites of amyloid plaques in Alzheimer's disease. Brain Res. 1996;717:173-178.

    Not in our library10.1016/0006-8993(95)01526-4

  94. 94.

    Nash B., Ioannidou K., Barnett S.C. Astrocyte phenotypes and their relationship to myelination. J. Anat. 2011;219:44-52.

    Not in our library10.1111/j.1469-7580.2010.01330.x

  95. 95.

    Nash B., Thomson C.E., Linington C., Arthur A.T., McClure J.D., McBride M.W., Barnett S.C. Functional duality of astrocytes in myelination. J. Neurosci. 2011;31:13028-13038.

    Not in our library10.1523/jneurosci.1449-11.2011

  96. 96.

    Nielsen S., Nagelhus E.A., Amiry-Moghaddam M., Bourque C., Agre P., Ottersen O.P. Specialized membrane domains for water transport in glial cells: high-resolution immunogold cytochemistry of aquaporin-4 in rat brain. J. Neurosci. 1997;17:171-180.

    Not in our library10.1523/jneurosci.17-01-00171.1997

  97. 97.

    Noble M., Murray K. Purified astrocytes promote the in vitro division of a bipotential glial progenitor cell. EMBO. J. 1984;3:2243-2247.

    Not in our library10.1002/j.1460-2075.1984.tb02122.x

  98. 98.

    Noble M., Murray K., Stroobant P., Waterfield M.D., Riddle P. Platelet-derived growth factor promotes division and motility and inhibits premature differentiation of the oligodendrocyte/type-2 astrocyte progenitor cell. Nature. 1988;333:560-562.

    Not in our library10.1038/333560a0

  99. 99.

    Noble M., Wolswijk G., Wren D. The complex relationship between cell division and the control of differentiation in oligodendrocyte-type-2 astrocyte progenitor cells isolated from perinatal and adult rat optic nerves. Prog. Growth Factor Res. 1989;1:179-194.

    Not in our library10.1016/0955-2235(89)90010-0

  100. 100.

    Odermatt B., Wellershaus K., Wallraff A., Seifert G., Degen J., Euwens C., Fuss B., Büssow H., Schilling K., Steinhäuser C., Willecke K. Connexin 47 (Cx47)-deficient mice with enhanced green fluorescent protein reporter gene reveal predominant oligodendrocytic expression of Cx47 and display vacuolized myelin in the CNS. J. Neurosci. 2003;23:4549-4559.

    Not in our library10.1523/jneurosci.23-11-04549.2003

  101. 101.

    Okada S., Nakamura M., Katoh H., Miyao T., Shimazaki T., Ishii K., Yamane J., Yoshimura A., Iwamoto Y., Toyama Y., Okano H. Conditional ablation of Stat3 or Socs3 discloses a dual role for reactive astrocytes after spinal cord injury. Nat. Med. 2006;12:829-834.

    Not in our library10.1038/nm1425

  102. 102.

    Omari K.M., John G.R., Sealfon S.C., Raine C.S. CXC chemokine receptors on human oligodendrocytes: implications for multiple sclerosis. Brain. 2005;128:1003-1015.

    Not in our library10.1093/brain/awh479

  103. 103.
    Cholesterol: Its Regulation and Role in Central Nervous System Disorders · 2012
    No notice
  104. 104.

    Pannasch U., Vargová L., Reingruber J., Ezan P., Holcman D., Giaume C., Syková E., Rouach N. Astroglial networks scale synaptic activity and plasticity. Proc. Natl. Acad. Sci. 2011;108:8467-8472.

    Not in our library10.1073/pnas.1016650108

  105. 105.

    Parpura V., Basarsky T.A., Liu F., Jeftinija K., Jeftinija S., Haydon P.G. Glutamate-mediated astrocyte-neuron signalling. Nature. 1994;369:744-747.

    Not in our library10.1038/369744a0

  106. 106.

    Pellegri G., Rossier C., Magistretti P.J., Martin J.L. Cloning, localization and induction of mouse brain glycogen synthase. Brain Res. Mol. Brain Res. 1996;38:191-199.

    Not in our library10.1016/0169-328x(95)00305-c

  107. 107.

    Pfeiffer-Guglielmi B., Fleckenstein B., Jung G., Hamprecht B. Immunocytochemical localization of glycogen phosphorylase isozymes in rat nervous tissues by using isozyme-specific antibodies. J. Neurochem. 2003;85:73-81.

    Not in our library10.1046/j.1471-4159.2003.01644.x

  108. 108.

    Pfrieger F.W., Ungerer N. Cholesterol metabolism in neurons and astrocytes. Prog. Lipid Res. 2011;50:357-371.

    Not in our library10.1016/j.plipres.2011.06.002

  109. 109.

    Porter J.T., Mccarthy K.D. Astrocytic neurotransmitter receptors in situ and in vivo. Prog. Neurobiol. 1997;51:439-455.

    Not in our library10.1016/s0301-0082(96)00068-8

  110. 110.

    Pringle N., Collarini E.J., Mosley M.J., Heldin C.H., Westermark B., Richardson W.D. PDGF A chain homodimers drive proliferation of bipotential (O-2A) glial progenitor cells in the developing rat optic nerve. EMBO. J. 1989;8:1049-1056.

    Not in our library10.1002/j.1460-2075.1989.tb03472.x

  111. 111.

    Pulver M., Carrel S., Mach J.P., De Tribolet N. Cultured human fetal astrocytes can be induced by interferon-gamma to express HLA-DR. J. Neuroimmunol. 1987;14:123-133.

    Not in our library10.1016/0165-5728(87)90047-6

  112. 112.

    Raff M.C., Miller R.H., Noble M. A glial progenitor cell that develops in vitro into an astrocyte or an oligodendrocyte depending on culture medium. Nature. 1983;303:390-396.

    Not in our library10.1038/303390a0

  113. 113.

    Raff M.C., Lillien L.E., Richardson W.D., Burne J.F., Noble M.D. Platelet-derived growth factor from astrocytes drives the clock that times oligodendrocyte development in culture. Nature. 1988;333:562-565.

    Not in our library10.1038/333562a0

  114. 114.

    Ransohoff R.M., Hamilton T.A., Tani M., Stoler M.H., Shick H.E., Major J.A., Estes M.L., Thomas D.M., Tuohy V.K. Astrocyte expression of mRNA encoding cytokines IP-10 and JE/MCP-1 in experimental autoimmune encephalomyelitis. FASEB J. 1993;7:592-600.

    Not in our library10.1096/fasebj.7.6.8472896

  115. 115.

    Rash J.E., Yasumura T., Hudson C.S., Agre P., Nielsen S. Direct immunogold labeling of aquaporin-4 in square arrays of astrocyte and ependymocyte plasma membranes in rat brain and spinal cord. Proc. Natl. Acad. Sci. 1998;95:11981-11986.

    Not in our library10.1073/pnas.95.20.11981

  116. 116.

    Redwine J.M., Armstrong R.C. In vivo proliferation of oligodendrocyte progenitors expressing PDGFalphaR during early remyelination. J. Neurobiol. 1998;37:413-428.

    Not in our library10.1002/(sici)1097-4695(19981115)37:3<413::aid-neu7>3.0.co;2-8

  117. 117.

    Redwine J.M., Blinder K.L., Armstrong R.C. In situ expression of fibroblast growth factor receptors by oligodendrocyte progenitors and oligodendrocytes in adult mouse central nervous system. J. Neurosci. Res. 1997;50:229-237.

    Not in our library10.1002/(sici)1097-4547(19971015)50:2<229::aid-jnr11>3.0.co;2-3

  118. 118.

    Rinholm J.E., Bergersen L.H. Neuroscience: the wrap that feeds neurons. Nature. 2012;487:435-436.

    Not in our library10.1038/487435a

  119. 119.

    Rinholm J.E., Hamilton N.B., Kessaris N., Richardson W.D., Bergersen L.H., Attwell D. Regulation of oligodendrocyte development and myelination by glucose and lactate. J. Neurosci. 2011;31:538-548.

    Not in our library10.1523/jneurosci.3516-10.2011

  120. 120.

    Rouach N., Koulakoff A., Abudara V., Willecke K., Giaume C. Astroglial metabolic networks sustain hippocampal synaptic transmission. Science. 2008;322:1551-1555.

    Not in our library10.1126/science.1164022

  121. 121.

    Rudge J.S., Pasnikowski E.M., Holst P., Lindsay R.M. Changes in neurotrophic factor expression and receptor activation following exposure of hippocampal neuron/astrocyte cocultures to kainic acid. J. Neurosci. 1995;15:6856-6867.

    Not in our library10.1523/jneurosci.15-10-06856.1995

  122. 122.

    Salehi Z., Hadiyan S.P., Navidi R. Ciliary neurotrophic factor role in myelin oligodendrocyte glycoprotein expression in cuprizone-induced multiple sclerosis mice. Cell. Mol. Neurobiol. 2013;33:531-535.

    Not in our library10.1007/s10571-013-9918-7

  123. 123.

    Sánchez-Abarca L.I., Tabernero A., Medina J.M. Oligodendrocytes use lactate as a source of energy and as a precursor of lipids. Glia. 2001;36:321-329.

    Not in our library10.1002/glia.1119

  124. 124.

    Schafer D.P., Lehrman E.K., Stevens B. The "quad-partite" synapse: microglia-synapse interactions in the developing and mature CNS. Glia. 2013;61:24-36.

    Not in our library10.1002/glia.22389

  125. 125.

    Schulz K., Kroner A., David S. Iron efflux from astrocytes plays a role in remyelination. 2012;32:4841-4847.

    Not in our library10.1523/jneurosci.5328-11.2012

  126. 126.

    Schwartz J.P., Nishiyama N. Neurotrophic factor gene expression in astrocytes during development and following injury. Brain Res. Bull. 1994;35:403-407.

    Not in our library10.1016/0361-9230(94)90151-1

  127. 127.

    Selmaj K., Raine C.S. Tumor necrosis factor mediates myelin damage in organotypic cultures of nervous tissue. Ann. N. Y. Acad. Sci. 1988;540:568-570.

    Not in our library10.1111/j.1749-6632.1988.tb27175.x

  128. 128.

    Selmaj K., Raine C.S., Cannella B., Brosnan C.F. Identification of lymphotoxin and tumor necrosis factor in multiple sclerosis lesions. J. Clin. Invest. 1991;87:949-954.

    Not in our library10.1172/jci115102

  129. 129.

    Siegel G.J., Agranoff B.W., Albers R.W., Fisher S.K., Uhler M.D. Basic Neurochemistry: Molecular, Cellular and Medical Aspects. 1999;1999.

    Not in our library

  130. 130.

    Silberstein F.C., De Simone R., Levi G., Aloisi F. Cytokine-regulated expression of platelet-derived growth factor gene and protein in cultured human astrocytes. J. Neurochem. 1996;66:1409-1417.

    Not in our library10.1046/j.1471-4159.1996.66041409.x

  131. 131.

    Sofroniew M.V., Vinters H.V. Astrocytes: biology and pathology. Acta Neuropathol. 2010;11:7-35.

    Not in our library10.1007/s00401-009-0619-8

  132. 132.

    Solenov E., Watanabe H., Manley G.T., Verkman A.S. Sevenfold-reduced osmotic water permeability in primary astrocyte cultures from AQP-4-deficient mice, measured by a fluorescence quenching method. Am. J. Physiol, Cell Physiol. 2004;286:C426-C432.

    Not in our library10.1152/ajpcell.00298.2003

  133. 133.

    Stankoff B., Aigrot M.S., Noël F., Wattilliaux A., Zalc B., Lubetzki C. Ciliary neurotrophic factor (CNTF) enhances myelin formation: a novel role for CNTF and CNTF-related molecules. J. Neurosci. 2002;22:9221-9227.

    Not in our library10.1523/jneurosci.22-21-09221.2002

  134. 134.

    Steinhäuser C., Jabs R., Kettenmann H. Properties of GABA and glutamate responses in identified glial cells of the mouse hippocampal slice. Hippocampus. 1994;4:19-35.

    Not in our library10.1002/hipo.450040105

  135. 135.

    Stöckli K.A., Lillien L.E., Näher-Noé M., Breitfeld G., Hughes R.A., Raff M.C., Thoenen H., Sendtner M. Regional distribution, developmental changes, and cellular localization of CNTF-mRNA and protein in the rat brain. J. Cell Biol. 1991;115:447-459.

    Not in our library10.1083/jcb.115.2.447

  136. 136.

    Swanson R.A., Ying W., Kauppinen T.M. Astrocyte influences on ischemic neuronal death. Curr. Mol. Med. 2004;4:193-205.

    Not in our library10.2174/1566524043479185

  137. 137.

    Tekkök S.B., Brown A.M., Westenbroek R., Pellerin L., Ransom B.R. Transfer of glycogen-derived lactate from astrocytes to axons via specific monocarboxylate transporters supports mouse optic nerve activity. J. Neurosci. Res. 2005;81:644-652.

    Not in our library10.1002/jnr.20573

  138. 138.

    Traugott U., Lebon P. Interferon-gamma and Ia antigen are present on astrocytes in active chronic multiple sclerosis lesions. J. Neurol. Sci. 1988;84:257-264.

    Not in our library10.1016/0022-510x(88)90130-x

  139. 139.
    Microglial Interactions with Synapses Are Modulated by Visual Experience · 2010
    No notice
  140. 140.

    Tress O., Maglione M., May D., Pivneva T., Richter N., Seyfarth J., Binder S., Zlomuzica A., Seifert G., Theis M., Dere E., Kettenmann H., Willecke K. Panglial gap junctional communication is essential for maintenance of myelin in the CNS. J. Neurosci. 2012;32:7499-74518.

    Not in our library10.1523/jneurosci.0392-12.2012

  141. 141.

    Tsukada N., Miyagi K., Matsuda M., Yanagisawa N., Yone K. Tumor necrosis factor and interleukin-1 in the CSF and sera of patients with multiple sclerosis. J. Neurol. Sci. 1991;104:230-234.

    Not in our library10.1016/0022-510x(91)90315-x

  142. 142.

    Uchida K., Baba H., Maezawa Y., Furukawa S., Furusawa N., Imura S. Histological investigation of spinal cord lesions in the spinal hyperostotic mouse (twy/twy): morphological changes in anterior horn cells and immunoreactivity to neurotropic factors. J. Neurol. 1998;245:781-793.

    Not in our library10.1007/s004150050287

  143. 143.

    Ullian E.M., Sapperstein S.K., Christopherson K.S., Barres B.A. Control of synapse number by glia. Science. 2001;291:657-661.

    Not in our library10.1126/science.291.5504.657

  144. 144.

    Vana A.C., Flint N.C., Harwood N.E., Le T.Q., Fruttiger M., Armstrong R.C. Platelet-derived growth factor promotes repair of chronically demyelinated white matter. J. Neuropathol. Exp. Neurol. 2007;66:975-988.

    Not in our library10.1097/nen.0b013e3181587d46

  145. 145.

    Vernerey J., Macchi M., Magalon K., Cayre M., Durbec P. Ciliary neurotrophic factor controls progenitor migration during remyelination in the adult rodent brain. J. Neurosci. 2013;33:3240-3250.

    Not in our library10.1523/jneurosci.2579-12.2013

  146. 146.

    Villarroya H., Violleau K., Ben Younes-Chennoufi A. Baumann N. Myelin-induced experimental allergic encephalomyelitis in Lewis rats: tumor necrosis factor alpha levels in serum and cerebrospinal fluid immunohistochemical expression in glial cells and macrophages of optic nerve and spinal cord. J. Neuroimmunol. 1996;64:55-61.

    Not in our library10.1016/0165-5728(95)00151-4

  147. 147.

    Voskuhl R.R., Peterson S., Song B., Ao Y., Morales L.B.R., Tiwari-Eoodruff S., Sofroniew M.V. Reactive astrocytes form scar-like perivascular barriers to leukocytes during adoptive immune inflammation of the CNS. J. Neurosci. 2009;29:11511-11522.

    Not in our library10.1523/jneurosci.1514-09.2009

  148. 148.

    Wallraff A., Köhling R., Heinemann U., Theis M., Willecke K., Steinhäuser C. The impact of astrocytic gap junctional coupling on potassium buffering in the hippocampus. J. Neurosci. 2006;26:5438-5447.

    Not in our library10.1523/jneurosci.0037-06.2006

  149. 149.

    Watkins T.A., Emery B., Mulinyawe S., Barres B.A. Distinct stages of myelination regulated by gamma-secretase and astrocytes in a rapidly myelinating CNS coculture system. Neuron. 2008;60:555-569.

    Not in our library10.1016/j.neuron.2008.09.011

  150. 150.

    Webster H.D., Shii H., Lassmann H. Immunocytochemical study of myelin-associated glycoprotein (MAG), basic protein (BP), and glial fibrillary acidic protein (GFAP) in chronic relapsing experimental allergic encephalomyelitis (EAE). Acta Neuropathol. 1985;65:177-189.

    Not in our library10.1007/bf00686996

  151. 151.

    Williams A., Piaton G., Lubetzki C. Astrocytes—friends or foes in multiple sclerosis? Glia. 2007;55:1300-1312.

    Not in our library10.1002/glia.20546

  152. 152.

    Winter C.G., Saotome Y., Levison S.W., Hirsh D. A role for ciliary neurotrophic factor as an inducer of reactive gliosis, the glial response to central nervous system injury. Proc. Natl. Acad. Sci. 1995;92:5865-5869.

    Not in our library10.1073/pnas.92.13.5865

  153. 153.

    Woodruff R.H., Fruttiger M., Richardson W.D., Franklin R.J. Platelet-derived growth factor regulates oligodendrocyte progenitor numbers in adult CNS and their response following CNS demyelination. Mol. Cell. Neurosci. 2004;25:252-262.

    Not in our library10.1016/j.mcn.2003.10.014

  154. 154.

    Wu Y., Dissing-Olesen L., MacVicar B.A., Stevens B. Microglia: dynamic mediators of synapse development and plasticity. Trends Immunol. 2015;36:605-613.

    Not in our library10.1016/j.it.2015.08.008

  155. 155.

    Xu Q., Bernardo A., Walker D., Kanegawa T., Mahley R.W., Huang Y. Profile and regulation of apolipoprotein E (ApoE) expression in the CNS in mice with targeting of green fluorescent protein gene to the ApoE locus. J. Neurosci. 2006;26:4985-4994.

    Not in our library10.1523/jneurosci.5476-05.2006

  156. 156.

    Yamamuro A., Ago Y., Takuma K., Maeda S., Sakai Y., Baba A., Matsuda T. Possible involvement of astrocytes in neuroprotection by the cognitive enhancer T-588. Neurochem. Res. 2003;28:1779-1783.

    Not in our library10.1023/a:1026103304490

  157. 157.

    Yong V.W., Moumdjian R., Yong F.P., Ruijs T.C., Freedman M.S., Cashman N., Antel J.P. Gamma-interferon promotes proliferation of adult human astrocytes in vitro and reactive gliosis in the adult mouse brain in vivo. Proc. Natl. Acad. Sci. U.S.A. 1991;88:7016-:7020.

    Not in our library10.1073/pnas.88.16.7016

  158. 158.

    Yoshida M., Saito H., Katsuki H. Neurotrophic effects of conditioned media of astrocytes isolated from different brain regions on hippocampal and cortical neurons. Experientia. 1995;51:133-136.

    Not in our library10.1007/bf01929356

  159. 159.

    Zamanian J.L., Xu L., Foo L.C., Nouri N., Zhou L., Giffard R.G., Barres B.A. Genomic analysis of reactive astrogliosis. J. Neurosci. 2012;32:6391-6410.

    Not in our library10.1523/jneurosci.6221-11.2012

  160. 160.

    Zhu, Z.H., Yang, R., Fu, X., Wang, Y.Q., Wu, G.C. 2006. Astrocyte-conditioned medium protecting hippocampal neurons in primary cultures against corticosterone-induced damages via PI3-K/Akt signal pathway. Brain Res. 1114, 1–10.

    Not in our library10.1016/j.brainres.2006.07.070

Cited by papers we hold 8

Reads

Read by people on this page

None yet.

Checked or read by AI through naulon

None yet.

A person counts once a day per paper. We keep no cookie and no address: a reader is a hash that changes every day. Any month under five reads shows no number.

Are you an author?

Is this your paper?

Claim it to add your note and be paid when agents cite it. Free.