摘要:

AbstractIn a previous study we demonstrated that differentiation and development of mouse oligodendrocytes is similar to that of the rat after the stage at which O4 is acquired. In this present study we compare directly the early differentiation of oligodendrocytes in the mouse and rat post natal optic nerve and show that the two species differ at the O‐2A progenitor and proligodendroblast stages. Mouse progenitors show a variety of morphologies compared to the typical bipolar appearance in the rat. Many murine cells fail to immunolabel with A2B5, GD3, O4, and RmAb, classical markers for rat progenitors, proligodendroblasts, and immature oligodendrocytes. We find that these “unlabeled” cells stain for GAP‐43 and that expression of GAP‐43 overlaps A2B5 and GD3 in the earlier progenitors and 04, RmAb, and 01 in the later proligodendroblasts and immature oligodendrocytes.Our data suggest that in the development of the mouse O‐2A progenitor cells there is a developmental discontinuity between the earlier markers such as A2B5 and GD3 and the later marker O4, which can be filled by GAP‐43. We therefore consider that GAP‐43 could be used in the mouse, in addition to the classical O‐2A markers, for the study of the early oligodendrocyte lineage as it labels an otherwise undetectable O‐2A population. ©

ISSN:0894-1491    

DOI:10.1002/glia.440150202

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

年代:1995

数据来源: WILEY

摘要:

AbstractThe present study aimed to characterize the reaction of mammalian (rat) retinal macroglia (Müller cells and astrocytes) to disturbances of their environment in the form of intraorbital section of the optic nerve, intraocular insertion of a thin glass capillary (without damage to the retina) or a combination of both. Glial reactivity was assessed through the use of a battery of antibodies which recognise four different proteins—glial fibrillary protein (GFAP) and three other proteins designated repectively MA1, 4D6 and 4H11. Retinal astrocytes did not exhibit any changes in normally expressed GFAP or MA1. By contrast, the expression of GFAP and MA1 in Müller cells increased 14 days following section of the optic nerve and/or intravitreal insertions of a glass capillary. Three days postoperatively, the expression of GFAP, but not MA1, had already increased significantly in Müller cells. 4D6 and 4H11 proteins were not expressed in astrocytes. In Müller cells, the levels of these proteins increased significantly following combined optic nerve section and intraocular insertion of a glass capillary. Thus, a mechanical disturbance of the intraocular environment constitutes a more effective stimulus in increasing the expression of some Müllerian proteins than damage to the axons of retinal ganglion cells. Such changes have important implications for various ocular treatments that involve intraocular administration of drugs, as well as for the survival/regeneration potential of retinal ganglion cells undergoing Wallerian degeneration. © 1995 Wiley‐

ISSN:0894-1491    

DOI:10.1002/glia.440150203

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

年代:1995

数据来源: WILEY

摘要:

AbstractThe increased expression of immunoreactive endothelin‐1 (ET‐1) in reactive astrocytes and its mitogenic effects on astrocytes and glioma cell lines, have implicated endothelins in the development of reactive gliosis. In this study, an increase in DNA synthesis in rat type I astrocytes was observed after cultures were transiently exposed to ET‐1 for 15 min, suggesting that early signal transduction events are essential and sufficient for the propagation of the ET‐1‐induced mitogenic signal. Prompt increases in inositol triphosphate (IP3) formation and [Ca2+]iwere observed upon the addition of ET‐1 to these cells. The ET‐1‐evoked increase in [Ca2+]iconsisted of an initial peak which was preserved in Ca2+‐free medium, and a sustained phase which was abolished in Ca2+‐free medium and partly attenuated by nifedipine. ET‐1 also increased the activity of membrane‐associated protein kinase C (PKC) and induced the in vivo phosphorylation of the 85 kD MARCKS protein, an endogenous PKC‐specific substrate. The ET‐1‐evoked increases in DNA synthesis, IP3, [Ca2+]i, membrane PKC, and 85 kD MARCKS protein phosphorylation in rat cortical astrocytes were prevented by either the selective endothelin ETAreceptor antagonist, BQ‐123, or the phospholipase C (PLC)‐specific inhibitor, U‐73122. However, the inhibition of PKC activity did not affect ET‐1‐induced DNA synthesis in rat cortical astrocytes. These results suggest that ET‐1‐induced IP3and/or [CA2+]iresponses, but not the activation of PKC, are essential for the growth‐factor like actions of ET‐1 in

ISSN:0894-1491    

DOI:10.1002/glia.440150204

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

年代:1995

数据来源: WILEY

摘要:

Abstract“Perineuronal nets” (PNs) ensheath a subtype of inhibitory neurons in the mammalian neocortex. In the light of the proposal that PNs consist of glial processes, we have analyzed the relationship between intracellularly injected glial cells and PNs in the rat neocortex. Glial cells were injected iontophoretically with Lucifer Yellow in lightly fixed tissue slices and PNs were visualized with the lectin from Vicia villosa. Using confocal laser scanning microscopy, glial processes and PNs were identified as distinct structures. Lectin labeling was consistently associated with the extracellular space interposed between LY‐labeled astrocyte processes and neurons. Of the different types of glial cells injected, only the densely‐ramifying protoplasmic astrocytes extended processes which could be traced to contact PNs. These protoplasmic astrocytes also sent out processes to adjacent neurons not ensheathed by PNs, and to capillaries. The present data strongly suggests that PNs do not consist of glial processes but rather support the idea that PNs represent specialized extracellular material interposed between the surface of some inhibitory interneurons and astrocytic processes. © 1995 Wiley

ISSN:0894-1491    

DOI:10.1002/glia.440150205

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

年代:1995

数据来源: WILEY

摘要:

AbstractThe amyloid precursor protein (APP) is rapidly induced in reactive glial cells in response to several pathological stimuli including inflammation. In the present study, observations previously made in animal models of autoimmune central nervous system inflammation have been extended to the analysis of multiple sclerosis (MS) lesions. A total of thirty fresh‐frozen tissue blocks from six histopathologically normal control and six MS cases have been examined immunocytochemically with monoclonal antibodies directed against either C‐ or N‐terminal epitopes of APP. Histopathological evaluation of disease progression was based on hematoxylin‐eosin and oil red O staining and immunocytochemistry for T cells, macrophages/microglia, astrocytes, and oligodendrocytes. In control cases, APP immunoreactivity was generally low and confined to blood vessel walls, oligodendrocytes in white, and neurons in grey matter. In actively demyelinating plaques, however, levels of APP immunoreactivity were high, localised on T lymphocytes, foamy macrophages, activated microglia, and reactive astrocytes including astrocytic processes. In more chronic lesions, levels of APP immunoreactivity were generally lower than in acute lesions, mainly found on reactive astrocytes, their processes and a few macrophages/microglia depending on the stage of plaque development. In addition, a few 14E‐positive oligodendrocytes and, moreover, numerous axons exhibited APP immunoreactivity, which was particularly pronounced with anti‐C‐terminal antibodies. These results demonstrate that APP is induced on reactive glial cells but also on T lymphocytes during demyelination. The extent of APP expression appears to be correlated to histopathological lesion development and thus suggests that APP detection serves as a sensitive marker for disease progression in MS. © 1995 W

ISSN:0894-1491    

DOI:10.1002/glia.440150206

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

年代:1995

数据来源: WILEY

摘要:

AbstractIn the present report we describe the effect of glutamate on respiratory activity in primary cultures of astrocytes, derived from cerebral cortex of newborn rat.Glutamate (100 μM) caused an increased oxygen consumption. This effect could not be inhibited by antagonists to the NMDA or AMPA/kainate receptors. Neither trans‐ACPD (an agonist to the metabotropic glutamate receptor) nor the Krebs cycle intermediate α‐ketoglutarate had any effect on the respiratory rate. An uncontrolled influx of Na+, caused by gramicidin, could mimic the glutamate effect on respiratory activity. In addition, the glutamate effect was abolished by addition of ouabain or replacement of Na+by Li+in the perfusion buffer.We conclude that the co‐transport of Na+, in the Na+‐dependent high‐affinity glutamate uptake system, mediated the glutamate‐induced increase in oxygen consumption through an increased activity of Na+/K+‐ATPases. © 1995

ISSN:0894-1491    

DOI:10.1002/glia.440150207

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

年代:1995

数据来源: WILEY

摘要:

AbstractIn the present study we analyze the events which occur during the early stages of astrogliogenesis by examining the pattern of both GFAP and vimentin gene expression and their corresponding immunoreactive proteins during rat brain development. This study was carried out “in vivo” (whole brain) and “in vitro” (primary culture of radial glia) using immunofluorescence, immunoblotting, and Northern blot analysis. Our results demonstrate that although GFAP immunostaining appeared late in gestation and at day 5 in radial glia cultures, GFAP mRNA expression was first detected, at very low levels, on fetal (F) day 15 and increased to F21. During postnatal development a striking increase in GFAP and its encoding messenger occurs. In contrast, the levels of vimentin and its mRNA expression were very high during the fetal stage (F15 to F21). Thereafter vimentin expression declined during postnatal (P) development until P21 and then remained constant at adult levels. In contrast, an increase in vimentin expression was observed in glial cells throughout the entire culture period. The biological significance of the developmental patterns of GFAP and vimentin expression in astroglial cells during brain development is discussed. © 1995 Wiley

ISSN:0894-1491    

DOI:10.1002/glia.440150208

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

年代:1995

数据来源: WILEY

摘要:

AbstractWe have evaluated the role of nitric oxide (NO) on the cyclooxygenase pathway in mouse glial cells. Exposure of primary cultures of neonatal mouse cortical astrocytes to bacterial lipopolysaccharide (LPS; 1 μg/ml, 18 h) caused an increase in the release of both nitrite (NO−2) and prostaglandin E2(PGE22), products of NO synthase (NOS) and cyclooxygenase, respectively. Production of both, NO−2and PGE2by astrocytes, was inhibited by the exposure of the NOS inhibitor Nw‐nitro‐L‐arginine methyl ester (L‐NAME: 1, 10, and 100 μM) in a dose related manner. Besides, other NOS inhibitors such as Nitro L‐arginine (NNA: 10−3M) prevented the increase in PGE2release from LPS‐stimulated astrocytes. Sodium nitroprusside (SNP; 100–200 μM) used as a NO donor caused a dose‐related enhancement in the accumulation of PGE2induced by LPS and the presence of hemoglobin blocked the SNP effects. The exposure to SNP counteracted the decrease of PGE2production in LPS‐treated astrocytes in which NO synthesis was blocked by L‐NAME. In addition, SNP also enhanced the synthesis of PGE2following exogenous arachidonic acid astrocytes exposure. Interestingly, this effect was blocked by indomethacin. Treatment of astrocytes cultures with dexamethasone (0.1, 1 μM) blocked dose‐relatedly the LPS‐induced release of both NO−2and PGE2. As expected, the presence of indomethacin (1, 10, and 20 μM) prevented in a dose related fashion, PGE2production by astrocytes following exposure to LPS. These results strongly indicate that in astroglial cells, NO is able to activate the cyclooxyge

ISSN:0894-1491    

DOI:10.1002/glia.440150209

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

年代:1995

数据来源: WILEY

摘要:

AbstractThe relative contribution of voltage activated Na+and K+currents to the whole cell current pattern of hippocampal glial cells was analyzed and compared during different stages of postnatal maturation. The patch‐clamp technique was applied to identified cells in thin brain slices obtained from animals between postnatal day 5 and 35 (p5‐35). We focused on a subpopulation of glial cells in the CA1 stratum radiatum which most probably represents a pool of immature astrocytes, termed “complex” cells. These cells could not be labelled by 01/04 antibodies, but some of the older cells were positively stained for glial fibrillary acidic protein (GFAP). In the early postnatal days, the current pattern of the “complex” cells was dominated by two types of K+outward currents: a delayed rectifier and a transient component. In addition, all cells expressed significant tetrodotoxin (TTX)‐sensitive Na+currents. During maturation, the contribution of delayed rectifier and A‐type currents significantly decreased. Furthermore, almost all cells after p20 lacked Na+currents. This down‐regulation of voltage gated Na+and K+outward currents was accompanied by a substantial increase in passive and inward rectifier K+conductances. We found increasing evidence of electrical coupling between the “complex” cells with continued development. It is concluded that these developmental changes in the electrophysiological properties of “complex” glial cells could be jointly responsible for the well known impaired K+homeostasis in the early postnatal hippocampu

ISSN:0894-1491    

DOI:10.1002/glia.440150210

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

年代:1995

数据来源: WILEY

摘要:

AbstractMouse sciatic nerves from the degeneration‐resistant strain C57BL/6/Wld (Ola) were surgically injected with lysolecithin to induce focal demyelination. Three days later they were transected adjacent to the spinal cord to eliminate contact of the axons with their cell bodies. The Na+channel distribution was assessed by immunocytochemistry and followed at several stages of remyelination. Control experiments were performed on nerves that were injected but not cut. At (3+4) days, namely, nerves cut 3 days post‐injection and examined 4 days after cutting, axons contained fully demyelinated regions. Na+channel clusters appeared only at heminodes and at isolated sites that are likely to represent original nodes of Ranvier. During the next few days proliferating Schwann cells adhered to the axons and extended their processes. Clusters of Na+channels appeared at their edges, and as the Schwann cells elongated the distance between these aggregates increased. A few clusters associated with neighboring Schwann cells approached each other and appeared to coalesce at sites where presumably new nodes of Ranvier would be formed. Beyond (3+6) days excessive degeneration of the transected axons precluded further observations. In the uncut controls, the spatio‐temporal sequence of Schwann cell proliferation and channel patch formation and movement was similar to that described above, although myelin formation was somewhat faster than in the cut axons. It is concluded that Na+channel aggregation associated with the early stages of remyelination is not dependent upon continuous communication of the axon with its cell body and is under local control. © 1995 Wiley‐L

ISSN:0894-1491    

DOI:10.1002/glia.440150211

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

年代:1995

数据来源: WILEY