摘要:

AbstractNeurogenesis in the olfactory epithelium continues throughout the entire life of mammals, and it is the axons of these newly formed olfactory receptor neurons that grow into the target tissue after the first cranial nerve is injured, not the regenerating axons of mature cells. These axons are able to enter and grow within the CNS of adult animals, unlike regenerating axons in injured dorsal roots, the majority of which are prevented from penetrating very far into the spinal cord. One reason why the olfactory axons are so successful in entering the CNS may be due, at least partially, to the fact that they are ensheathed by a type of glial cell (the ensheathing cell) that expresses phenotypic features of both astrocyte and Schwann cells. The presence of both L1/Ng‐CAM and N‐CAM in the plasma membranes of both ensheathing cells and immature olfactory receptor neurons would enable the olfactory axons to use the glial cell surfaces as a substratum on which to grow. It is probably also true that ensheathing cells synthesize and secrete laminin, thus providing an additional adhesive substrate for the olfactory axons, as well as glia‐derived nexin and nerve growth factor, both of which are neuritepromoting a

ISSN:0894-1491    

DOI:10.1002/glia.440030602

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

年代:1990

数据来源: WILEY

摘要:

AbstractBrain slices were incubated with either [3H] amino acids or [32P] orthophosphate in order to characterize the synthesis and phosphorylation of the glial fibrillary acidic protein (GFAP) in the rat nervous system. The incorporation of [3H] amino acids into GFAP was found to increase significantly during early postnatal development, reaching a peak of activity on day 5 of life and then declining over the next 2 weeks. Concomitant with this peak of synthetic activity the content of GFAP in rat brain was also observed to increase dramatically. GFAP continued to accumulate in brain through postnatal day 30 despite a decrease in the synthesis of the protein. These results indicate that the increase in GFAP during the first month of life cannot be ascribed solely to the rate of GFAP synthesis. The findings are consistent with the hypothesis that during later stages of astrocytic development the accumulation of GFAP may be primarily dependent upon a low rate of protein degradation. The pattern of GFAP phosphorylation in the developing rat brain differed from that observed for the incorporation of [3H] amino acids. The peak incorporation of32P into GFAP occurred on postnatal day 10 at a time when synthesis of the protein had declined by 43%. These findings suggest that during development phosphorylation of GFAP is mediated by factors different from those directing its synthesis. In addition, phsophorylation of GFAP did not alter its solubility in cytoskeletal preparations indicating that GFAP phosphorylation is probably not a major regulatory mechanism in disassembly of the astroglial filaments.

ISSN:0894-1491    

DOI:10.1002/glia.440030603

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

年代:1990

数据来源: WILEY

摘要:

AbstractOral administration of thioridazine, an inhibitor of peroxisomal β‐oxidation, to normal rats from weaning till day 60 causes a small increase of the very long chain fatty acid C26 in brain lipids. Myelination in the brain is decreased. In the genu of the corpus callosum the ratio of non‐myelinated/myelinated axons is increased. In the commissura anterior the myelin sheaths of the axons are significantly thinner in treated than in control animals. Undernourishment caused by the drug is minimal in this experiment. Area and total DNA of glial nuclei are unaltered in both the genu and the commissura anterior of treated rats. The distribution of chromatin (texture), however, shows small differences in the corpus call

ISSN:0894-1491    

DOI:10.1002/glia.440030604

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

年代:1990

数据来源: WILEY

摘要:

AbstractIn the Royal College of Surgeons rat with inherited retinal dystrophy, photoreceptor cell degeneration is accompanied by retinal pigment epithelial (RPE) cell alterations and Müller cell changes such as increased expression of glial fibrillary acidic protein (GFAP). Vascular changes such as vascularization of the RPE, vascular proliferation, and formation of vitreoretinal membranes (VRMs) are observed later. To study the relationship of Müller cell changes to the vascular alterations in the dystrophic retina, we used immunoperoxidase techniques and antibodies against GFAP and vimentin. Our study showed that during photoreceptor degeneration, Müller cells expressed small amounts of GFAP. As degeneration progressed, GFAP expression increased and morphological alterations occurred in Müller cells. Müller cell apical processes extended and proliferated in the subretinal space and contacted the apical surface of duplicated RPE cells. Later, GFAP reactive fibers surrounded retinal vessels apposed to the RPE. As the vessels became enmeshed within the RPE, the GFAP‐positive perivascular processes disappeared. Eventually, the RPE‐associated vessels became displaced into the inner retina where VRMs were sometimes observed. Immunoblots showed increased GFAP in dystrophic as compared with control retinas. Studies of vimentin distribution in the dystrophic retina showed results similar to the GFAP study. Moreover, the vimentin study suggested increased number of Müller cell processes in the dystrophic as compared with control retinas. The close temporal and anatomical relationships among Müller cell, RPE, and vascular changes in the dystrophic rat suggest a role for Müller cells in retinal neovascularization and proliferative

ISSN:0894-1491    

DOI:10.1002/glia.440030605

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

年代:1990

数据来源: WILEY

摘要:

AbstractAstrocytic response in the immediate vicinity of freeze‐ and cobalt‐induced lesions has been examined at the light and ultrastructural level. However, the temporal and spatial distribution of astrocytic reactivity throughout the rat cerebral cortex, using glial fibrillary acidic protein (GFAP) immunolabeling, has not been examined. The first purpose of this study was to establish the chronological distribution of astrocytic reactivity, as measured by changes in GFAP immunoreactivity, following freeze‐ or cobalt‐induced injury to the rat cerebral cortex. Cobalt metal also has been proposed to have a direct effect on astrocytes and has been shown to stimulate in vitro astrocytes to become reactive. The second purpose of this report was to determine if cobalt had an effect on in vitro astrocytic gap junctional dye coupling as measured by fluorescence recovery after laser‐photobleaching (gap‐FRAP). Although the chronological development of the increased GFAP immunoreactivity was different for the freeze‐ and cobalt‐induced lesions, astrocytes initially showed an increase in GFAP immunoreactivity in the region surrounding these lesions. This initial response was followed by a spread of increased GFAP immunoreactivity throughout certain regions of the ipsilateral cerebral hemisphere and then by a restriction of the increased immunolabeling to the lesion site. Cobalt also had a direct effect on in vitro astrocytes as demonstrated by the inhibition of astrocytic gap junctional dye coupling. Based on gap‐FRAP analysis, cobalt significantly blocked fluorescence recovery (2.5%) as compared to the fluorescence recovery in control astrocytes (26%). It is proposed that the initial increase in GFAP immunoreactivity may be due to decreased gap ju

ISSN:0894-1491    

DOI:10.1002/glia.440030606

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

年代:1990

数据来源: WILEY

摘要:

AbstractThe cat visual cortex develops its mature appearance, i.e., its circuitry and neuronal morphology, during a limited period of postnatal development under the influence of visual experience. The critical period for cortical plasticity, which normally extends from the third to seventh postnatal week, can be prolonged by raising animals in total darkness. The prolongation of the critical period by dark‐rearing is restricted to the cortical layers except layer IV. Besides the influence of afferent activity on the physiology of cortical cells and on the interconnectivity of thalamo‐cortical afferents, visual experience has also been shown to affect the development of glial cells. The present study investigates the effects of dark‐rearing on astroglial characteristics as determined by immunostaining for glial fibrillary acidic protein (GFAP) and the S‐100 protein. The data reveal a retardation of astrocytic maturation in dark‐reared animals, shown by a reduced presence of GFAP immunoreactivity compared to light‐experienced animals. The density of astrocytic cell bodies positive for S‐100 is unaffected by dark‐rearing, suggesting that astroglial proliferation does not rely on afferent activity. However, punctate S‐100 staining in the neuropil, which has been shown to reflect astrocytic processes, was also reduced in certain cortical layers in dark‐reared animals. The effects of dark‐rearing on the expression of GFAP and S‐100 were restricted to the cortical layers except layer IV, i.e., those layers that reveal a prolongation of the critical period for cortical plasticity following dark‐rearing. It is concluded that astrocytic maturation in the visual cortex is influenced by neuronal activity. The coincidence of the location of retarded astrocytic maturation and the prolongation of the critical period for cortical plasticity is discussed in the light of the recent evidence that immature astrocytes may be involved in activity‐dependent plas

ISSN:0894-1491    

DOI:10.1002/glia.440030607

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

年代:1990

数据来源: WILEY

摘要:

AbstractGlial cells were isolated from the cerebra of 7‐day‐old rats and maintained in culture in a chemically defined medium that favours the development of oligodendrocytes. Acetate, butyrate, or albumin‐bound hexanoate, octanoate, decanoate, laurate, myristate, palmitate, oleate, linoleate, or arachidonate was added to the culture medium. The incorporation of [3H]acetate into fatty acids and cholesterol and [35S]sulphate into sulphatide, and the activities of the oligodendrocyte marker enzymes 2′,3′‐cyclic‐nucleotide 3′‐phosphodiesterase and glycerol 3‐phosphate dehydrogenase were measured. The composition of the glial cell population (the number of astrocytes and oligodendrocytes) in these cultures was studied by immunocytochemistry. Results show that 1) long‐chain fatty acids depress the synthesis of fatty acids, cholesterol, and sulphatide; and 2) the presence of long‐chain, in contrast to short‐chain, fatty acids in the culture medium lowers the activities of 2′,3′‐cyclic‐nucleotide 3′‐phosphodiesterase and glycerol 3‐phosphate dehydrogenase and decreases the number of oligodendrocytes. Our results suggest that long‐chain fatty acids exert a negative influence on the development of ol

ISSN:0894-1491    

DOI:10.1002/glia.440030608

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

年代:1990

数据来源: WILEY

摘要:

AbstractReactive gliosis was revealed by immunocytochemistry using antibodies against the glial fibrillary acidic protein (GFAP) after a stab or an electrolytic lesion administered to the cerebral cortex, corpus callosum, striatum, or hippocampus of a 6‐day‐old rat. The intensity of the gliosis was about the same in the various structures injured and did not change with the delay of 3, 7, or 20 days between the injury and the sacrifice of the animals. When basic fibroblast growth factor (bFGF) was injected in the lesion locus just after the lesion was performed, it resulted (as soon as 3 days after injury) in a strong astrogliosis that was enhanced after a delay of 7 days, the astrocytes in the lesion area exhibiting enlarged cell processes and intense GFAP‐positive immunoreactivity. After a delay of 20 days, the astrocytes were not dispersed any more but packed in three or four layers along the borders of the lesion, thus reducing its extension. This suggests a possible role for bFGF in promoting scar formation following brain i

ISSN:0894-1491    

DOI:10.1002/glia.440030609

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

年代:1990

数据来源: WILEY

摘要:

AbstractBasic fibroblast growth factor (bFGF) is a potent mitogen for several types of cells, including glial cells, which also seem to express bFGF. We have used rat C6 glioma cells as a model system to study the expression and release of bFGF by glioma cells, as well as the effects of exogenous bFGF on these cells. We have shown that C6 cells, express 18 kD bFGF and several higher molecular weight immunoreactive forms. The expression of bFGF could be induced by a factor present in fetal calf serum. Subsequent to its initial appearance, bFGF is regulated in a cell density‐dependent manner. Neither bFGF‐like immunoreactive material, nor bFGF‐like neurotrophic activity were found to be released by C6 cells. Exogenously applied bFGF changed C6 cell morphology similar to cyclic AMP induced alterations but had no significant influence on C6 cell proliferation and biochemical differentiation. From these results we conclude that bFGF in C6 cells might act as an endogenous (not autocrine) mitogen. Possible roles for bFGF in glial cells are disc

ISSN:0894-1491    

DOI:10.1002/glia.440030610

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

年代:1990

数据来源: WILEY

摘要:

AbstractAspects of hyperglycemic ischemia were simulated in cultures of astrocytes and of neurons by high glucose and dinitrophenol exposure. Lactate release increased almost sevenfold and it was found that astrocytes were responsible for 92% of the release. There was no significant increase in internal lactate content. Experiments involving loading of astrocytes with lactate at different external pH values showed that lactate accumulation was increased by an increased inward proton gradient. This inward transport of lactate probably consists of two transport components, a passive diffusion of its neutral form and transport via a recently described monocarboxylic acid carrier. It was found that lactate did not get trapped in astrocytes, despite the fact that loading of astrocytes with lactic acid by exposure to 30 mM lactic acid increased the membrane input resistance dramatically. We conclude that lactate is released as lactic acid from astrocytes and equilibrates quickly with all CNS compartments. Thus we argue against a role of lactate accumulation in cytotoxic swelling.

ISSN:0894-1491    

DOI:10.1002/glia.440030611

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

年代:1990

数据来源: WILEY