摘要:

AbstractNumerous ectopic granule cells are found in the molecular layer of the dentate gyrus in NZB/BINJ and dreher mutant mice. These ectopic neurons occur either singly or in small clusters. In contrast, few ectopic granule cells are seen in the dentate molecular layer of C57BL/6J mice and dreher control littermates. In this investigation we have examined the morphology, number, and distribution of molecular layer astrocytes in NZB/BINJ, dreher homozygotes, dreher littermate controls, and C57BL/6J mice to determine the effect of the presence of ectopic granule cells. In the molecular layer of C57BL/6J mice and dreher control littermates, astrocytes have a typical stellate appearance with processes emanating in all directions. The arborization of astrocytes in areas devoid of ectopic granule cells in NZB/BINJ mice and dreher homozygotes was similar to that in C57BL/6J mice and dreher control littermates. In contrast, the morphology of astrocytes in the immediate vicinity of ectopic granule cells or ectopic clusters was distinctly non‐stellate. Furthermore, the somata and processes of these astrocytes occasionally appeared to make intimate contact with the ectopic granule cells. A quantitative analysis of the number and distribution of astrocytes in NZB/BINJ vs C57BL/6J mice and dreher vs. control littermates indicated that these parameters were not altered by the presence of the ectopic neurons. We conclude that the trophic effects of ectopic neurons on glial cells can affect the growth and orientation of astrocytic processes without a concomitant effect on glial cell number. © 1994 Wiley‐Liss,

ISSN:0894-1491    

DOI:10.1002/glia.440100102

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

年代:1994

数据来源: WILEY

摘要:

AbstractTreatment of rat C6 glioma cells with the tricyclic antidepressant desipramine induces opioid binding. Here the distribution of these opioid‐binding sites on C6 cell membranes and a functional property were investigated. Immunohistochemical examination of C6 cells was performed using a monoclonal anti‐idiotypic antibody to opioid receptors (Ab2AOR). Ab2AOR uniformly labeled>97% of the cells exposed to desipramine over their entire surface. The opioid‐receptor antagonist naltrexone completely blocked Ab2AOR binding. Ab2AOR, which has opioid agonist properties, also inhibited DNA synthesis in desipramine‐treated but not in naive C6 cells. Similarly, morphine blocked C6 cell proliferation only after desipramine treatment. The antineurotrophic action of Ab2AOR was reversed by naltrexone and was insensitive to pertussis toxin. These findings demonstrate that Ab2AOR suppresses the proliferation of C6 glioma cells by binding to desipramine‐induced opioid receptors. © 1994 Wiley

ISSN:0894-1491    

DOI:10.1002/glia.440100103

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

年代:1994

数据来源: WILEY

摘要:

AbstractThe poor regenerative ability of neurons of the central nervous system in mammals, as compared with their counterpart in fish or amphibians, is thought to stem from differences in their immediate nonneuronal environment and its response to axonal injury. We describe one aspect of the environmental response to axonal injury in a spontaneously regonerating system‐the fish optic nerve. The aspect under investigation was the reaction of glial cells at the injury site. This was examined by the use of antibodies that specifically recognize vimentin in fish glial cells. In the present study, affinity‐purified vimentin antibodies were raised against a nonconserved N‐terminal 14‐amino acid peptide, which was predicted from the nucleotide sequence of vimentin. These antibodies were found to react specifically with glial cells in vitro. Moreover, the antivimentin antibodies stained both the optic nerve and the optic tract, but with different patterns. Specificity of the antibodies was verified by protein immunoblotting, tissue distribution, and labeling patterns. After injury, vimentin immunoreactivity initially disappeared from the site of the lesion due to cell death. Early signs of glial cell migration toward the injury site were evident a few days later. It is suggested that the reappearance of vimentin‐positive glial cells at the site of injury is associated with axonal elongation across it, and that they contribute to the regenerative ability of the fish optic nerve. © 1994 Wiley

ISSN:0894-1491    

DOI:10.1002/glia.440100104

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

年代:1994

数据来源: WILEY

摘要:

AbstractThe cell cycle encompasses the sequential events regulating cell division. In mammalian brain, initiation of astrocyte cycling is critical during development and injury. To investigate the timing of growth factor requirements as they commit to passing through the G1phase, primary and secondary rat astrocytes were stimulated to enter the cycle after serum or growth factor deprivation. Bromodeoxyuridine immunofluorescence was used to monitor S phase nuclei after growth factor re‐addition (at time 0). Cycle kinetics were identical whether quiescent cultures were exposed to 10% (vol/vol) calf serum, or to a defined medium containing fibroblast growth factor, insulin, and epidermal growth factor. The control point in late G1that represents commitment to achieving the G1/S transition was identified by cycloheximide (CHX, 0.1 μg/ml) addition. Sensitivity to cycle arrest by CHX disappeared at 9–10 h. In contrast, shift‐down to growth factor‐deficient medium arrested cell cycling virtually until G1/S (12 h). With selective exposure during late G1(9–12 h), no single agent permitted cycle progression. However, any two agents enabled cycling, and complementary or synergistic effects were apparent. These requirements were identical in astroglia from newborn and long‐term cultures.Thus, temporal dissociation exists between the processes of escape from CHX sensitivity and from requirements for growth factors, two recognized hallmarks of commitment to cycle progression. Furthermore, simultaneous presence of at least two growth factors is necessary at or near G1/S. Both findings distinguish astrocytes from several other cell types. © 1994 Wi

ISSN:0894-1491    

DOI:10.1002/glia.440100105

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

年代:1994

数据来源: WILEY

摘要:

AbstractWe have discovered that a strongly fluorescent dye, sulforhodamine 101, when injected intravitreally in vivo, very effectively stains a class of star‐shaped cells in the innermost layers of the rabbit retina. The cells were strictly confined to the region containing medullated fibers and emitted dichotomously branching processes that ended up running some distance along the myelinated fibers. In favorable cases they could be seen to ensheath the fibers in a tube‐like fashion. No other retinal cells were stained. Shortly (hours) after the injection, the stain appeared in the cell cytoplasm, but it later became progressively more localized to intracellular granules. Most of the dye had disappeared after 2 days.Oligodendrocytes and astrocytes are the only cells known to be confined to the region of the medullated fibers in the rabbit retina, and hence the sulforhodamine 101‐stained cells should be one of these two types. Sulforhodamine 101‐stained cells were indistin‐guishable from oligodendrocytes identified by 2′,3′‐cyclic nucleotide phosphodiesterase (CNP) immunohistochemistry, and sequential staining showed them to be the same. Sulforhodamine 101‐stained cells were microinjected with lucifer yellow after lightly fixing rabbit retinas with formaldehyde and were found to be indistinguishable from oligodendrocytes. Glial fibrillary acidic protein staining for astrocytes showed fiber bundles that to some extent were similar to the bundles stained by sulforhodamine 101, but at the level of individual fibers, it was impossible to establish any concordance. Sulforhodamine 101 thus appears to stain oligodendrocytes rather than astrocytes in the rabbit retina.A related dye, rhodamine 123, also stained rabbit oligodendrocytes, but with poor contrast because many other cells and structures were also stained. A number of related rhodamine dyes did not stain the rabbit oligodendrocytes.The staining procedure is simple, has wide tolerance margins, gives robust results, and is well suited for cell microinjections and similar experiments. © 19

ISSN:0894-1491    

DOI:10.1002/glia.440100106

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

年代:1994

数据来源: WILEY

摘要:

AbstractTo study beneficial effects of immature astrocytes on axonal regeneration in the injured adult mammalian brain, we have stereotactically implanted cultured astrocytes from embryonic (E 14–16) rat cerebral cortex into the lesion site following transection of the postcommissural fornix. The spatio‐temporal pattern of axonal degeneration and regrowth in the proximal fornix stump was investigated using wheat germ agglutinin‐horseradish peroxidase tracing techniques and quantitative analysis of myelinated axon profiles.Transection of the postcommissural fornix tract caused disintegration of the axons in the distal stump as well as rapid and pronounced retrograde axonal degeneration up to 800–1,200 μm proximal to the lesion site. While a small bundle of subicular fibers spontaneously extended to the lesion site within 4 weeks after injury, axonal regeneration was markedly stimulated in those animals that had received an astroglial implant. Following the former pathway, regenerating axons sprouted towards the implant but did not penetrate the graft. Instead, the axons elongated over the surface of the transplant, avoiding growth into the surrounding neuropil or into the distal fornix segment. In grafted animals we further observed a substantial increase in the number of myelinated axons of approximately 31.5% (at the level of 800 μm) and approximately 40% (at the 400 μm level) compared with the injured tract lacking a transplant. Our results indicate the capacity of juvenile astrocytes to stimulate axonal regeneration after injury of the post‐commissural fornix tract in the adult rat brain. We further demonstrate myelination of the regenerated axons. © 1994 Wi

ISSN:0894-1491    

DOI:10.1002/glia.440100107

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

年代:1994

数据来源: WILEY

摘要:

AbstractThe influence of gonadal steroids on the ultrastructure of glial cells and on the immunoreactivity for the specific astrocytic marker glial fibrillary acidic protein (GFAP) has been assessed in the neuroendocrine hypothalamus. The following parameters were analyzed in the arcuate nucleus of adult female rats: the number and the surface density of cells immunoreactive for GFAP, the number of glial profiles showing bundles of glial filaments, the size of the bundles of glial filaments, and the proportion of neuronal perikaryal membrane apposed by glial processes. These parameters were studied during the different phases of the estrous cycle, after ovariectomy, and after the administration of estradiol or progesterone to ovariectomized rats. No significant differences were detected in the number of GFAP‐immunoreactive cells among the different experimental groups. The surface density of GFAP‐immunoreactive material, the number of glial profiles in the neuropil, and the proportion of neuronal perikaryal membrane covered by glia were increased in the afternoon of proestrus and in the morning of estrus compared with other phases of the estrous cycle or to ovariectomized rats and showed a rapid (5 h) and reversible increase in ovariectomized rats injected with 17β estradiol, with a maximal effect by 24 h after the administration of the hormone. In contrast, the size of the bundles of glial filaments was decreased in the afternoon of proestrus, in the morning of estrus, and by the administration of estradiol to ovariectomized rats. The parameters studied were not affected by the administration of progesterone. However, progesterone (300 μg/rat) blocked the effects of 17β estradiol (1, 10, and 300 μg). The results suggest that glial cells may be actively involved in the modulation of neuroendocrine events by the hypothalamus. © 1994 Wiley

ISSN:0894-1491    

DOI:10.1002/glia.440100108

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

年代:1994

数据来源: WILEY

摘要:

AbstractSchwann cell‐axon contacts in developing and regenerating peripheral nerve in situ contain high levels of the recognition molecules L1 and N‐CAM, while the molecules are not detectable at the ab‐axonal cell surface of Schwann cells. To investigate whether Schwann cells, axons, or both contribute to the localization of the molecules at Schwann cell‐axon contacts, a heterologous cell culture system consisting of Schwann cells from mice and neurons from chicken was investigated by immunoelectron microscopy using species‐specific L1 and N‐CAM antibodies. We showed that Schwann cells expressed both molecules only at sites of contact between Schwann cells and neurites and other Schwann cells. Schwann cells not in contact with other cells expressed both molecules on their entire cell surface. In contrast, neurites expressed G4, an L1‐related molecule in chicken, on their entire cell surface independently of whether they were in contact with other cells or not. Thus, cultured Schwann cells localize L1 and N‐CAM selectively at cell contact sites and may thereby stabilize their attachment to the neighboring cellular partners. © 1994

ISSN:0894-1491    

DOI:10.1002/glia.440100109

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

年代:1994

数据来源: WILEY

摘要:

AbstractIncubation of C6 glioma cells in the presence of aminoglutethimide, an inhibitor of cholesterol metabolism, together with either adenosine 3′,5′‐cyclic monophosphate (cAMP) analogues or agents that increase cAMP synthesis, such as cholera toxin, forskolin, and isoproterenol, stimulated the rate of pregnenolone formation by their isolated mitochondria. This effect of cAMP was blocked by the antagonist (Rp)‐cAMPS. The incorporation rate of mevalonolactone into pregnenolone was also increased by the stimulation of adenylyl cyclase activity in intact C6 cells. It is concluded that cAMP stimulates glial cell steroidogenesis by increasing the movement of the substrate, cholesterol, to the mitochondria, where it will be metabolized to pregnenolone by the side chain cleavage cytochrome P450 enzyme. © 1994 Wiley

ISSN:0894-1491    

DOI:10.1002/glia.440100110

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

年代:1994

数据来源: WILEY

ISSN:0894-1491    

DOI:10.1002/glia.440100111

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

年代:1994

数据来源: WILEY