摘要:

AbstractThis review summarizes the current scientific literature concerning the ependymal lining of the cerebral ventricles of the brain with an emphasis on selective barrier function and protective roles for the common ependymal cell. Topics covered include the development, morphology, protein and enzyme expression including reactive changes, and pathology. Some cells lining the neural tube are committed at an early stage to becoming ependymal cells. They serve a secretory function and perhaps act as a cellular/axonal guidance system, particularly during fetal development. In the mature mammalian brain ependymal cells possess the structural and enzymatic characteristics necessary for scavenging and detoxifying a wide variety of substances in the CSF, thus forming a metabolic barrier at the brain‐CSF interface. © 1995 Wiley‐Liss,

ISSN:0894-1491    

DOI:10.1002/glia.440140102

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1995

数据来源: WILEY

ISSN:0894-1491    

DOI:10.1002/glia.440140103

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1995

数据来源: WILEY

摘要:

AbstractCalcium imaging techniques were used to study intracellular free calcium ion regulation in isolated Müller cells in response to changes in extracellular potassium concentration and to caffeine and ryanodine. Müller cells were dissociated from the adult tiger salamander (Ambystomatigrinum) retina and studied using the calcium indicator Fura‐2 and video imaging microscopy techniques. Our results demonstrate that elevation of extracellular potassium in the presence of extracellular calcium evokes an increase in intracellular calcium ([Ca2+]i) throughout the length of the Müller cell. In contrast, in the absence of extracellular calcium, elevation of extracellular potassium can trigger a long latency, wave‐like increase in [Ca2+]ithat begins in the apical region of the Müller cell and moves toward the endfoot. A similar calcium wave can be evoked in Müller cells when they are exposed to caffeine or ryanodine, agents that cause release of calcium from intracellular stores in many cell types. These data suggest that [Ca2+]imay be altered in Müller cells through an extracellular pathway as well as through a ryanodine‐sensitive intracellular release mechanism. The functional consequences of these changes in [Ca2+]iremain to be elucidated. © 1995 Wil

ISSN:0894-1491    

DOI:10.1002/glia.440140104

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1995

数据来源: WILEY

摘要:

AbstractIn the normal rat retina the Thy‐1 antigen is a specific marker of ganglion cells, but degeneration of ganglion cells in vivo does not remove completely the expression of Thy‐1 in the retina. To reconcile these differences we have postulated that ganglion cell death could induce a glial response including the expression of Thy‐1 in Müller cells, the main glial cell type in the retina. Using immunocytochemistry, we have shown that pure cultures of Müller cells were strongly labelled with antibodies against Thy‐1. PCR amplification of cDNA reverse transcribed from Müller cell RNA indicated the presence of Thy‐1 transcripts. Double labelling experiments with anti‐Thyl and anti‐glutamine synthetase, a marker of Müller cells, indicated the presence of both antigens in the same cells. Although Müller cells expressed Thy‐1 mRNA and protein when cultured in the absence of neuronal cells, when co‐cultured with retinal neurons they were not labelled with antibodies against Thy‐1. Our results suggest that Thy‐1 is expressed by Müller cells following loss of retinal neurons. Thy‐1 may have an important function during glial response to neuron death in r

ISSN:0894-1491    

DOI:10.1002/glia.440140105

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1995

数据来源: WILEY

摘要:

AbstractThe mature oligodendrocyte, though able to divide under certain circumstances, has been regarded as incapable of changing into a phenotypically plastic cell type. To further explore this question, we developed an in vitro system in which a virtually pure population of early postnatal canine oligodendrocytes were cultured in a serum free, defined medium. We tested the oligodendrocytes' morphological and mitotic responses to concentration of basic Fibroblast Growth Factor (bFGF) ranging from 5 ng to 100 ng/ml. We found that bFGF effected both the morphology and mitotic potential of these cells. In addition, oligodendrocytes exposed to bFGF respond to 10% fetal bovine serum (FBS) by undergoing morphological changes that are quite different than naive oligodendrocytes exposed to 10% FBS, suggesting that bFGF causes some fundamental change in plasticity. © 1995 Wiley‐Liss, I

ISSN:0894-1491    

DOI:10.1002/glia.440140106

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1995

数据来源: WILEY

摘要:

AbstractHuman and monkey brain sections were examined by immunohistochemical light and electron microscopy to determine the distribution of GLUT1, a glucose transporter isoform associated with erythrocytes and endothelial cells of the human blood‐brain barrier. Protein immunoblotting of fractionated human brain membranes was performed to determine the distribution of molecular forms of the transporter. GLUT1 staining was abundant in erythrocytes and cerebral endothelium of gray and white matter but was also present diffusely in gray matter neuropil when viewed by light microscopy. Immunoelectron microscopy confirmed the gray matter and vascular localization of GLUT1, with specific GLUT1 staining seen in erythrocytes, gray and white matter endothelial cells, astrocyte foot processes surrounding gray matter blood vessels, and in astrocyte processes adjacent to synaptic contacts. No astrocytic staining was identified in white matter. Astrocyte GLUT1 staining was identified only in mature gray matter regions; undifferentiated regions of preterm (22–23 weeks gestation) cortex had GLUT1 staining only in blood vessels and erythrocytes, as did germinal matrix. Immunoblots of adult human frontal cortex revealed that two forms of GLUT1 (45 and 52 kDa) were present in unfractionated brain homogenates. Immunoblots of vessel‐depleted frontal lobe revealed only the 45 kDa form in gray matter fractions, and depleted in membranes prepared from white matter regions. We conclude that the GLUT1 isoform of glucose transporter is present both in endothelium of the blood‐brain barrier and in astrocytes surrounding gray matter blood vessels and synapses. Furthermore, the form present in astrocytes is likely to have a lower molecular weight than the form found in cerebral endothelium. The GLUT1 transporter may play an important role not only in astrocyte metabolism, but also in astrocyte‐associated pathways supporting neuronal energy metabolism. © 1995 Wiley

ISSN:0894-1491    

DOI:10.1002/glia.440140107

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1995

数据来源: WILEY

摘要:

AbstractCorpora amylacea (CA) are cytoplasmic inclusions that accumulate in human brain in the course of normal aging, and to an even greater extent, in Alzheimer's disease and other neurodegenerative conditions. In senescent and Alzheimer‐diseased human brains, astrocytes in limbic and periventricular regions exhibit red autofluorescent inclusions, homologous to Gomori‐positive astrocyte granules previously described in the brains of aging rodents and other vertebrates. We have shown that Gomori inclusions in situ and in culture are derived from autophagocytosed mitochondria exhibiting iron‐mediated peroxidase activity. In the human brain, the autofluorescent inclusions share many properties with CA. Both types of inclusion progressively accumulate in periventricular regions with advancing age, are largely astrocytic in origin, and contain various heat shock proteins and ubiquitin. Using histochemistry in conjunction with confocal microscopy, we demonstrated that both CA and the red autofluorescent granules exhibit non‐enzymatic peroxidase activity and an affinity for CAH and PAS. The only major divergent histochemical feature between the Gomori‐positive astrocyte granules and CA is the presence of orange‐red autofluorescence in the former and the absence of endogenous fluorescence in the latter. On the basis of numerous shared topographic and histochemical features, we hypothesized that CA are largely derived from autofluorescent (Gomori‐positive) astrocyte granules which reside in periventricular regions of the senescent CNS. Immunofluorescent labeling and laser scanning confocal microscopy demonstrated consistent colocalization of the mitochondrial proteins, sulfite oxidase, and heat shock protein 60, to both CA and the autofluorescent astroglial inclusions. In addition, both CA and the autofluorescent astrocyte granules exhibit staining for DNA which colocalizes to mitochondrial antigens and therefore likely represents mitochondrial nucleic acid in dual‐labeled preparations. These observations suggest that a) Gomori‐positive astrocyte granules in human brain are homologous to those described in rodents, b) Gomori‐positive granules may be structural precursors of CA in senescent human brain, and c) in the aging human brain, degenerate mitochondria within periventricular astrocytes give rise to autofluorescent cytoplasmic granules and corpora amylacea. ©

ISSN:0894-1491    

DOI:10.1002/glia.440140108

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1995

数据来源: WILEY

摘要:

AbstractRecent evidence indicates that astroglia may be involved in the synthesis of endogenous neurosteroids. The extension of glial fibrillary acidic protein (GFAP)‐immunoreactive astroglial cell processes was assessed in hippocampal slice cultures from adult gonadectomized male rats under the influence of the neurosteroids dehydroepiandrosterone, dehydroepiandrosterone sulfate, dehydroepiandrosterone estereate, pregnenolone, pregnenolone sulfate, and pregnenolone oleate. The effects of neurosteroids were compared to those induced by the gonadal steroids testosterone, 17ß‐estradiol and progesterone. Astrocytes in hippocampal slice cultures had a morphology that was indistinguishable from that observed in the hippocampus fixed in situ. Castration of adult male rats resulted in a significant decrease in the extension of GFAP‐immunoreactive processes, both in tissues fixed in situ and in slice cultures. In contrast, incubation of slice cultures from gonadectomized animals with pregnenolone, pregnenolone sulfate, 17ß‐estradiol, and testosterone enhanced the extension of GFAP‐immunoreactive processes. While other steroids tested did not affect this parameter, dehydroepiandrosterone and its sulfate and estereate derivatives induced the transformation of astroglial cells into hypertrophic and highly GFAP immunoreactive cells with the morphological characteristics of reactive astroglia. We conclude that neurosteroids regulate the morphology and/or GFAP distribution of astrocytes in hippocampal slice cultures from adult rats. © 1995 Wil

ISSN:0894-1491    

DOI:10.1002/glia.440140109

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1995

数据来源: WILEY

ISSN:0894-1491    

DOI:10.1002/glia.440140110

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1995

数据来源: WILEY

ISSN:0894-1491    

DOI:10.1002/glia.440140101

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1995

数据来源: WILEY