bluuebunny/crossref_metadata_2025_split huggingface dataset:
Media that support the growth and differentiation of oligodendrocytes do not induce olfactory ensheathing cells to express a myelinating phenotype
Authors: Doucette R. , Devon R. 
Published: May 2005

AbstractThe glial cells that ensheath olfactory axons are referred to as ensheathing cells. In vivo, these non‐myelinating glial cells express a mixture of astrocyte‐specific and Schwann cell‐specific phenotypic features with the former cellular phenotype predominating, but in vitro can assemble a myelin sheath when co‐cultured with dorsal root ganglion neurons. Thus, certain in vitro conditions induce ensheathing cells to express a phenotype more like that of a myelinating Schwann cell. The present study addresses whether ensheathing cells will express a myelinating phenotype in neuron‐free cultures when fed for 1 to 5 weeks with media shown to promote the growth and differentiation of oligodendrocyte progenitor cells. The ensheathing cell cultures were initiated using the nerve fiber layers (NFL) of rat olfactory bulb primordia. Oligodendrocyte cultures were established from newborn rat neopallium and from the tissue that remained after removing the NFL from the developing olfactory bulb (i.e., the OB‐NFL). The cultures were double‐labelled with rabbit polyclonal antibodies to S100 or glial fibrillary acidic protein in combination. With the mouse monoclonal antibodies 04, BRD1 [anti‐galactocerebroside (anti‐GAL‐C)], and anti‐myelin basic protein (MBP). In some experiments the ensheathing cells were labelled with PKH26 prior to being co‐cultured with oligodendrocytes of the OB‐NFL. None of the media induced ensheathing cells to express either GAL‐C or MBP. However, when 0.5 mM dibutyrylcyclic‐AMP (dBcAMP) was added to the medium, ensheathing cells became GAL‐C + ve, but remained MBP‐ve. The molecular mechanisms that regulate the expression of a myelinating phenotype by ensheathing cells appear to be different from those that operate in oligodendrocytes. © 1994 Wiley‐Liss, Inc.
Myelin‐associated glycoprotein is not detectable in perikaryal myelin of spiral ganglion neurons of adult mice
Authors: Martini Rudolf 
Published: May 2005

AbstractThe expression of the adhesion molecules N‐CAM (neural cell adhesion molecule), L1, myelin‐associated glycoprotein (MAG), and P0 has been investigated by postembedding‐immunoelectron microscopy in spiral ganglia of adult mice in which both axons and neuronal cell bodies are myelinated. L1 was absent from both axonal and perikaryal myelin of spiral ganglion neurons but was expressed on unmyelinated nerve fibers. P0 was expressed in compacted parts of both types of myelin but was absent from non‐compacted myelin. MAG was not detectable in perikaryal myelin but was strongly expressed in axonal myelin both periaxonally and in non‐compacted regions. Conversely, N‐CAM was detectable at the interface between myelin and neuronal perikarya and in non‐compacted regions of perikaryal myelin, whereas it was hardly detectable in axonal myelin. This inverse expression of MAG and N‐CAM in perikaryal and axonal myelin points to the possibility that N‐CAM may functionally replace MAG in perikaryal myelin of spiral ganglion neurons. © 1994 Wiley‐Liss, Inc.
Confocal imaging of glial cells in the intact rat optic nerve
Authors: Butt A. M. , Colquhoun K. , Berry M. 
Published: May 2005

AbstractAstrocytes and oligodendrocytes in the isolated intact mature rat optic nerve have been computer imaged in three dimensions by laser scanning confocal microscopy of single cells, dye‐filled with lysinated rhodamine dextran (LRD). Our results illustrate the first application of these techniques to an intact CNS white matter tract and provide comparative data for previous studies on neonatal rat optic nerve (Butt and Ransom: Glia 2:470–475,1989; Butt and Ransom: J Comp Neurol 338:141–158, 1993). The combined use of intracellular injection of LRD and confocal imaging significantly improves the resolution of glial cell structure, particularly that of mature astrocytes, for a number of reasons. (1) Single mature dye‐filled glia can be imaged, because LRD does not pass through gap junctions. (2) The entire process field of astrocytes can be visualized in a single two‐dimensional image. (3) Cell images can be rotated through 360° in all planes to provide a new perspective of glial cell structure in the intact tissue. (4) Reconstruction of optical sections, within a narrow focal plane, provides a high definition and resolution of the finer details of glial morphology. Using these techniques, three astrocyte subclasses were distinguished on morphological criteria. It is the conclusion of this study that the majority of these forms represent a single population of fibrous astrocytes which are well‐suited to perform the multiple functions attributed to astrocytes in the CNS. The morphology of mature myelin‐forming oligodendrocytes was also described. The results confirm that the structural characteristics of both astrocyte subtypes and oligodendrocytes described in younger rat optic nerves by Butt and Ransom (Glia 2:470–475,1989; J Comp Neurol 338:141–158, 1993) accurately reflect those of the mature glial population. © 1994 Wiley‐Liss, Inc.
Similarities and differences between fish oligodendrocytes and schwann cells in vitro
Authors: Bastmeyer Martin , Jeserich Gunnar , Stuermer Claudia A. O. 
Published: May 2005

AbstractIn light of the striking differences between oligodendrocytes of the optic nerve/tract of adult goldfish and their mammalian counterparts, a further characterization of goldfish oligodendrocytes was performed. A comparison with Schwann cells was included because fish optic nerve/tract‐derived oligodendrocytes bear remarkable similarities to this type of glial cell. Fish optic nerve/tract‐derived oligodendrocytes that had differentiated into 04 and 6D2‐positive cells and thus expressed early myelin marker molecules were found to incorporate BrdU and to divide in vitro over a period of weeks. For the induction of more advanced markers of myelinogenesis such as the CNS‐specific myelin protein 36K, oligodendrocytes required extensive contact with axons. Other agents, such as fetal calf or carp serum, substrate components, or forscolin failed, however, to induce 36K expression. 04/6D2‐positive oligodendrocytes could be distinguished from fish 6D2‐positive Schwann cells derived from cranial nerves by their antigenic pheno‐type: Schwann cells but not oligodendrocytes exhibited the low affinity NGF receptor. While both cell types carry the cell adhesion molecules NCAM, E 587 antigen, and the L2/HNK‐1 epitope, only Schwann cells possess a further adhesion molecule, Neurolin. © 1994 Wiley‐Liss, Inc.
Astrocytes exhibit regional specificity in gap‐junction coupling
Authors: Lee Sung H. , Kim Warren T. , Cornell‐Bell Ann H. , Sontheimer Harald 
Published: May 2005

AbstractAstrocytes are coupled to each other via gap‐junctions both in vivo and in vitro. Gap‐junction coupling is essential to a number of astrocyte functions including the spatial buffering of extracellular K+ and the propagation of Ca2+ waves. Using fluorescence recovery after photo‐bleach, we quantitatively assayed and compared the coupling of astrocytes cultured from six different central nervous system (CNS) regions in the rat: spinal cord, cortex, hypothalamus, hippocampus, optic nerve, and cerebellum. The degree of fluorescence recovery (% recovery) and time constant of recovery (∼) served as quantitative indicators of coupling strength. Gap‐junction coupling differed markedly between CNS regions. Coupling was weakest in astrocytes derived from spinal cord (43% recovery, τ∼400 s) and strongest in astrocytes from optic nerve (91% recovery, τ∼226 s) and cerebellum (95% recovery, τ∼100 s). As indicated by the degree of recovery, coupling strength among CNS regions could be ranked as follows: spinal cord < cortex < hypothalamus < hippocampus = optic nerve = cerebellum. Gap‐junction coupling also differed between CNS regions with respect to its sensitivity to inhibition by the uncoupling agent octanol. Kd values for 50% inhibition by octanol ranged from 188 μM in spinal cord astrocytes to 654 μM in hippocampal astrocytes. Sensitivity of gap‐junctions to octanol could be ranked as follows: spinal cord = cortex = hypothalamus> cerebellum> optic nerve> hippocampus. The observed differences in coupling indicate differences in the number of gap‐junction connections in astrocytes cultured from the six CNS regions. These differences may reflect the adaptation of astrocytes to varying functional requirements in different CNS regions. © 1994 Wiley‐Liss, Inc.
Fura‐2 signals evoked by kainate in leech glial cells in the presence of different divalent cations
Authors: Munsch Thomas , Nett Wolfgang , Deitmer Joachim W. 
Published: May 2005

AbstractThe glutamate‐agonist kainate evokes Ca2+ transients in both neurones and glial cells. Owing to the membrane depolarization elicited by kainate, a Ca2+ influx could occur through voltage‐gated Ca2+ channels or through the kainate‐gated cation channels directly. We have measured ratio signals of the calcium indicator dye fura‐2, injected into giant glial cells of the leech Hirudo medicinalis, as response to kainate (5‐20μ) in the presence of different divalent cations. The responses to kainate increased during the first 2‐4 kainate applications, both in unclamped and in voltage‐clamped cells. The fura‐2 fluorescence ratio (F 350/F380) still increased when Ca2+ was replaced by Ba2+ but was suppressed in Ca2+ ‐free saline and in the presence of Ni2+ (2 mM). Co2+ and Mn2+ (2 mM) also reduced the kainate‐induced fura‐2 fluorescence signals, due to entry of these divalent cations into the cells and subsequent quenching the fluorescence of the intracellular dye. It is concluded that Ni2+ blocks the kainate‐induced membrane depolarization and Ca2+transient but apparently does not enter the cells, while Ba2+, Co2+, and Mn2+ appear to permeate the membrane, presumably through the kainategated channels. © 1994 Wiley‐Liss, Inc.
Experimental gliopathy in the adult rat CNS: Effect on the blood‐spinal cord barrier
Authors: Krum Janette M. 
Published: May 2005

AbstractThe expression of certain blood‐brain barrier (BBB) properties in CNS endothelial cells appear to be dependent on astroglial interactions in vitro. However, evidence for direct astroglial support of BBB function in vivo is controversial. To determine if perivascular astroglial damage or loss would compromise BBB function in situ, localized astroglial degeneration was produced in adult rat spinal cords by systemic injections of the anti‐metabolite 6‐aminonicotinamide (6‐AN). Between 1 and 5 days after 6‐AN administration microvessels in the lumbar spinal cord (blood‐spinal cord barrier) were examined for the expression of several BBB markers and for leakage of endogenous and exogenous proteins by means of immunocytochemical and histochemical procedures. Glial cells throughout the gray matter were swollen after 24 h, and by 5 days post‐injection perivascular astroglia in laminae VI‐VIII appeared completely degenerated. Microvessels were undamaged and continued to express BBB markers such as GLUT‐I, ‐γ‐glutamyltranspeptidase, andendothelial barrier antigen in this region in a manner comparable to control animals. These results suggest that differentiated, BBB‐competent microvascular endothelia in situ may not depend on continuous astroglial support to maintain these particular BBB characteristics. However, the BBB to protein appeared to be compromised; the gray matter was immunoreactive for serum albumin and some areas were permeable to intravascularly injected horseradish peroxidase (HRP). No increase in microvascular transport vesicles was apparent, and no open, tracercontaining interendothelial junctions were detected using standard ultrastructural methods. Some venous structures were surrounded by hemorrhages and HRP reaction product. Thus, astrocytic injury may alter venous, and possibly microvascular, permeability to macromolecules. © 1994 Wiley‐Liss, Inc.
Trimethyltin‐induced expression of GABA and vimentin immunoreactivities in astrocytes of the rat brain
Authors: Andersson Helena , Luthman Johan , Olson Lars 
Published: May 2005

AbstractAdult Sprague‐Dawley rats were given a single dose of trimethyltin chloride (TMT). Three days following treatment, a neuronal alteration was observed in the CA3c pyramidal cell layer of hippocampus which was not accompanied by any apparent astrocyte reaction. At 1 as well as 2 weeks after treatment, a gliosis in hippocampus, piriform, and entorhinal cortices was detected by glial fibrillary acidic protein (GFAP) immunohistochemistry. Concomitant with the enhanced astrocytic GFAP, astrocytes were swollen and expressed immunoreactivity to vimentin and γ‐aminobutyric acid (GABA). The astrocytic GABA immunoreactivity may reflect a trimethyltin‐induced alteration in astrocyte phenotype, or alterations in compartmentalization and/or metabolism of GABA. © 1994 Wiley‐Liss, Inc.
Downregulation of in vitro neurotoxicity of brain macrophages by prostaglandin E2 and a β‐adrenergic agonist
Authors: Théry Clotilde , Dobbertin Alexandre , Mallat Michel 
Published: May 2005

AbstractBrain macrophages (BM), a subpopulation of microglia, have the ability to kill neurons by producing reactive oxygen intermediates. Cocultures of neurons and macrophages derived from the cerebral cortex of rat embryos were used to look for regulation ofBM neurotoxicity. Isoproterenol (10−7 M), a β‐adrenergic agonist, induced a significant inhibition of BM neurotoxicity and this effect was abolished in the presence of propranolol, a β‐adrenergic antagonist. BM neurotoxicity was also reduced in the presence of prostaglandin E2 (10−8, 10−6 M), a metabolite derived from arachidonic acid. These results suggest endogenous mechanisms of neuroprotection operating either during development or following lesions. © 1994 Wiley‐Liss, Inc.
Cortical type 2 astrocytes are not dye coupled nor do they express the major gap junction genes found in the central nervous system
Authors: Belliveau Daniel J. , Naus Christian C. G. 
Published: May 2005

AbstractThe O‐2A progenitor cell first described from the rat optic nerve is a bipotential precursor of oligodendrocytes and type 2 astrocytes. Each cell expresses specific markers that distinguish them as unique cell types. O‐2A progenitors cultured in high serum preferentially differntiate into type 2 astrocytes and when exposed to defined medium or low serum develop along the oligodendrocyte lineage. We analyzed the gap junction gene expression of type 2 astrocytes to determine if they are coupled to form a syncytium, like their type 1 astrocyte counterparts. Dye coupling experiments demonstrated that cortical type 2 astrocytes are not coupled, while type 1 astrocytes in the same culture dish are highly coupled. Immunocytochemistry revealed the presence of Cx43 in type 1 astrocytes but we could not detect Cx26, 32, or 43 protein in type 2 astrocytes. In situ hybridization did not detect mRNA for any of the three connexin genes in type 2 astrocytes. These data demonstrate that type 2 astrocytes do not express the major gap junction genes found in the central nervous system. The precise function of type 2 astrocytes is not known but the lack of gap junction genes expression suggests that their functions are different from the spatial buffering capacity of type 1 astrocytes.
A comparative Mac‐1 immunocytochemical and lectin histochemical study of microglial cells in the normal and athymic mice
Authors: Htain Wynn‐Wynn , Leong Seng‐Kee , Ling Eng‐Ang 
Published: May 2005

AbstractThe number of microglial cells in the supraventricular part of the corpus callosum stained with Mac‐1 antibody (against CR3 antigens) and the intensity of staining were studied in both the homozygous athymic nude mouse (nu/nu) and normal BALB/c mouse (+/+). For quantitative analysis, the mean microglial cell counts (expressed in terms of packing density) from 40 μm thick immunostained sections were obtained and tested by analysis of variance. The Mac‐1 positive cells in neonatal nude mice were slightly less intensely stained than those of their normal littermates. Such was not noticeable in the 13‐week‐ and 1‐year‐old animals. The mean number of immunopositive microglial cells per 0.0324 mm2 was significantly less in the 5‐day‐old (P < 0.001) and 13‐week‐old (P < 0.05) nude mice when compared to normal mice of corresponding ages. The difference was insignificant in the 1‐year‐old nude and normal mice. The distribution of Mac‐1 labelled lnicroglia in different areas of the brain of the postnatal nude and normal mouse was also examined. In the brain areas examined, e.g., the olfactory bulb, cerebral and cerebellar cortex, the number of microglia in the nude mouse was considerably reduced. The study of lectin labelled sections also showed a much smaller number of labelled microglial cells in the athymic mouse. This was especially obvious in the 5‐day‐old nude mouse when compared to the normal BALB/c mouse (P < 0.01). The lesser counts of microglia in athymic mice may be attributed to the lack of T lymphocytes and the thymus gland. The latter is known to produce thymic hormones especially thymosin, essential for the maturation of monocytes considered to be the precursor cells of microglia.
Human retinal microglia: Expression of immune markers and relationship to the Glia limitans
Authors: Provis Jan M. , Penfold Philip L. , Edwards Antony J. , van Driel Diana 
Published: May 2005

AbstractThe immunoreactivity, morphology and relationship to the glia limitans of microglia were investigated in flatmounts and sections of normal human retina, using immunogold histochemistry, electron microscopy (EM), and antibodies directed against CD45, major histocompatability complex class I (MHC‐I), MHC‐II, and human macrophage antigens. Immunoreactivity was evident for all antibodies tested, including MHC‐I, which labeled both microglia and retinal vascular endothelium. Most consistent labeling was obtained using antibodies to CD45, MHC‐II, and anti‐human macrophage (S22) antigen. Immunoreactive cells were seen in the perivascular space (perivascular cells), where they were closely adherent to the vessel profile, and in the retinal parenchyma (microglia). Some parenchymal microglia were also vessel associated and by EM were seen to be closely related to the glia limitans (paravascular microglia). Paravascular microglia were shown by optical densitometry, to express higher levels of MHC antigens than neighboring, non‐vessel associated, parenchymal microglia. In addition, paravascular microglia were macrophage (S22) antigen positive, while other parenchymal microglia did not express macrophage antigens. Quantitative data indicate that similar populations of microglia are immunoreactive to CD45, MHC‐I, and MHC‐II, while relatively few microglia (approximately 10%) are immunoreactive for human macrophage (S22) antigens, supporting previous suggestions that microglia are a heterogeneous population. © 1995 Wiley‐Liss, Inc.
Resident microglia and hematogenous macrophages as phagocytes in adoptively transferred experimental autoimmune transferred experimental autoimmune encephalomyelitis: An investigation using rat radiation bone marrow chimeras
Authors: Rinner W. A. , Bauer J. , Schmidts M. , Lassmann H. , Hickey W. F. 
Published: May 2005

AbstractHematogenous macrophages are known to be involved in the induction of tissue damage in the central nervous system (CNS) as well as of clinical symptoms in experimental autoimmune encephalomyelitis (EAE). Although resident microglia can become phagocytic under certain circumstances, little is known about the role of these cells in brain inflammation in vivo. We thus studied EAE in the model of radiation bone marrow chimeras that allows us to distinguish donor‐derived hematogenous cells from resident effector cells. Inflammation in the CNS was qualitatively and quantitatively similar in chimeras compared to fully histocompatible Lewis rats. Although activated resident microglial cells were outnumbered four‐to sevenfold in EAE lesions by hematogenous macrophages, the number of resident microglia with ingested myelin was equal to that of macrophages containing myelin debris. Phagocytic resident microglia, expressing the macrophage activation marker ED1, showed ramified as well as amoeboid morphology. From our studies the following conclusions can be drawn. First, a considerable proportion of resident microglia upregulated ED1. Second, resident microglia provide a small but substantial source of brain macrophages in EAE as compared to the large influx of macrophages. Third, our results suggest that macroglia, due to their strategic position within the CNS, are more effective in removal of myelin debris compared to hematogenous macrophages. © 1995 Wiley‐Liss, Inc.
Interleukin 1‐β‐ and tumor necrosis factor‐α‐mediated regulation of ICAM‐1 gene expression in astrocytes requires protein kinase C activity
Authors: Ballestas Mary E. , Benveniste Etty N. 
Published: May 2005

AbstractSeveral adhesion molecules including intracellular adhesion molecule‐1 (ICAM‐1) are expressed by astrocytes, the predominant glial cell of the central nervous system (CNS). Such molecules are important in the trafficking of leukocytes to sites of inflammation, and in lymphocyte activation. ICAM‐1 is constitutively expressed by neonatal rat astrocytes, and expression is enhanced by the proinflammatory cytokines interleukin‐1β (IL‐1β), tumor necrosis factor‐α (TNF‐α), and interferon‐γ (IFN‐γ), with IL‐1β and TNF‐α being the strongest inducers. In this study, we have examined the nature of the second messengers involved in ICAM‐1 gene expression induced by the cytokines IL‐1β and TNF‐α. Our results indicate that stimuli related to protein kinase C (PKC) such as the phorbol ester phorbol 12‐myristate 13‐acetate (PMA) and calcium ionophore A23187 increase ICAM‐1 mRNA expression, whereas cyclic nucleotide analogs and PKA agonists have no effect. Pharmacologic inhibitors of PKC such as H7, H8, and calphostin C inhibit ICAM‐1 gene expression inducible by IL‐1β and TNF‐α. Prolonged treatment of astrocytes with PMA results in a time‐dependent downregulating of the PKC isoforms α, δ, and ϵ, and a concomitant diminution of ICAM‐1 mRNA expression induced by IL‐1β, TNF‐α, and PMA itself at specific time points post‐PMA treatment. These data, collectively, demonstrate a role for various PKC isoforms in IL‐1β and TNF‐α enhancement of ICAM‐1 gene expression in rat astrocytes. © 1995 Wiley‐Liss, Inc.