bluuebunny/crossref_metadata_2025_split huggingface dataset:
Change of phosphotyrosine immunoreactivity on microglia in the rat substantia nigra following striatal ischemic injury
Authors: Korematsu Kojiro , Goto Satoshi , Nagahiro Shinji , Inoue Nobuhiro , Oyama Taro , Yamada Kazumichi , Ushio Yukitaka 
Published: December 2004

AbstractUsing immunohistochemistry, we investigated changes in phosphotyrosine (P‐Tyr) immunoreactivity on the microglia of the rat substantia nigra (SN) following striatal ischemic injury produced by transient middle cerebral artery (MCA) occlusion. Anterograde axonal degeneration in the SN due to striatal ischemic injury was detected by depletion of calcineurin immunoreactivity in that region from 1 day after operation. From 3 days to 1 month (the longest period examined in this study) after MCA occlusion, there was a significant increase in P‐Tyr immunoreactivity in the SN ipsilateral to the MCA occlusion. Also, light microscopic observation showed that the microglia exhibited an increased immunoreactivity for P‐Tyr and characteristic morphological changes in the ipsilateral SN. The present results indicate that a signal transducing cascade(s) associated with tyrosine phosphorylation may be involved in the activation of the microglia in the SN responding to anterograde degeneration of the striatonigral pathway. © 1995 Wiley‐Liss, Inc.
Effects of enhanced extracellular ammonia concentration on cultured mammalian retinal glial (müller) cells
Authors: Reichenbach A. , Stolzenburg J.‐U. , Wolburg H. , Härtig W. , El‐Hifnawi E. , Martin H. 
Published: December 2004

AbstractMüller (glial) cells of the neonatal rabbit retina were cultured as confluent monolayers and exposed to enhanced concentrations of ammonia (0.25, 0.5, 1, 3, 7, and IC mM) in medium for various periods (30 min to 10 d). This caused, in a time‐ and dose‐dependent manner, similar changes in the Müller cells as had previously been described in cultured astrocytes. The most conspicuous events were (1) an increasing size of cell nuclei, (2) an accumulation of phagocytotic vacuoles, and (3) a rearrangement of intermediate filaments. (4) A considerable number of cells died when higher ammonia concentrations were applied for more than 1 h. Simultaneous application of dibutyrylcyclic adenosine monophosphate (dBcAMP) prevented almost completely both the increase in cell nucleus size and the changes of intermediate filaments, but only partly the early cell death of a subpopulation of cells, and the accumulation of phagocytotic vacuoles. Further changes evoked by enhanced ammonia concentration were (5) an accumulation of lipofuscin‐like material (“fatty degeneration”) revealed by lipophilic stain, (6) reduced immunoreactivity for cathepsin D, and increased immunoreactivity for (7) glial fibrillary acidic protein, (8) glutamine synthetase, and (9) bcl‐2 protooncogene protein. These findings are discussed in respect to the possible underlying pathophysiological mechanisms. © 1995 Wiley‐Liss, Inc.
Estradiol promotion of changes in the morphology of astroglia growing in culture depends on the expression of polysialic acid of neural membranes
Authors: Garcia‐Segura Luis M. , Cañas Benito , Parducz Arpád , Rougon Geneviève , Theodosis Dionysia , Naftolin Frederick , Torres‐Aleman Ignacio 
Published: December 2004

AbstractGonadal steroids are known to affect astroglial morphology in developing and adult animals. Earlier studies of mixed neuronal‐glial cultures from fetal rat hypothalamus showed that glial fibrillary acidic protein (GFAP)‐immunoreactive cells with a polygonal shape were transformed into process‐bearing cells upon exposure to the ovarian hormone estradiol. This effect was dependent on a direct contact of astroglia with living hypothalamic neurons. The present study shows that somata and processes of neurons in such cultures were immunoreactive for polysialic acid (PSA); astroglia were immunonegative. PSA appears to participate in the estradiol‐induced shape changes since treatment with endoneuraminidase, an enzyme that specifically removes PSA from the cell surface, abolished PSA immunostaining and prevented the 17ß‐estradiol‐induced morphological changes of astroglia. In contrast, treatment with endoneuraminidase did not affect astroglial shape changes induced by basic fibroblast growth factor (bFGF), nor those induced by the addition of neurons to glial cultures. These results suggest that PSA on neuronal membranes, probably linked to the highly sialylated isoform of the neural cell adhesion molecule, is necessary for the expression of certain hormonally‐regulated neuro‐glial interactions. © 1995 Wiley‐Liss, Inc.
Boundaries and inhibitory molecules in developing neural tissues
Authors: Faissner Andreas , Steindler Dennis 
Published: December 2004

AbstractNumerous studies of the past decade have illuminated the importance of intercellular adhesion events for neural pattern formation. It has been documented that members of the Ig and cadherin gene superfamilies, that glycoproteins and, probably to some extent, proteoglycans of the extracellular matrix play a role in this context. Recent observations suggest that, in addition to adhesive interactions, repulsive and/or inhibitory phenoma are also of importance in regulating neural pattern formation. Several molecules are under study which are cosidered possible mediators of inhibitory interactions in the nervous system. The hypothesis has been advanced that some of these might be partially responsible for restrictive, boundary‐like properties ascribed to glial cells in developing and regenerating tissues. The current review summarizes these studies and focusses on molecular aspects of boundary and compartmentation phenomena. © 1995 Wiley‐Liss, Inc.
Behaviour of macroglial cells, as identified by their intermediate filament complement, during optic nerve regeneration of Xenopus tadpole
Authors: Rungger‐Brändle Elisabeth , Alliod Chantal , Fouquet Bernadette , Messerli Marius M. 
Published: December 2004

AbstractAssessment of glial cell behaviour during optic nerve (ON) regeneration in Xenopus tadpoles is hampered by the lack of classical cellular markers that distinguish different glial cells in mammals. We thus have characterized the intermediate filament (IF) complement of tadpole glial cells and used it to follow the fate of glial cell subsets during the first 10 days after ON crush. Glial cells synthesize a restricted number of cytokeratin (CK) species and vimentin. This pattern remains essentially unchanged during metamorphosis and regeneration. However, vimentin turnover is specifically enhanced after injury. The expression of CKs and vimentin has been followed immunocytochemically in situ and in isolated cells recovered from dissociated ON segments. In the normal nerve, 79% of ramified glial cells express both CK and vimentin, 1% CK and 4% vimentin only, whereas 16% express neither IF protein. We tentatively classified CK expressing cells as mature astrocytes and those without IF proteins as oligodendrocytes. In the regenerating ON, the relative number of oligodendrocytes is decreased, while the astrocytic subset becomes accordingly larger but is decreased by day 10 already in favour of cells expressing vimentin only. Astrocytes invade the lesion site soon after crush, arrange into a central core within the distal nerve segment and establish a peripheral scaffold that is readily crossed by axons. Unlike mammalian astrocytes that remain absent from the lesion site but form a scar at some distance to it, amphibian astrocytes appear to provide active guidance to axons growing through the lesion site. © 1995 Wiley‐Liss, Inc.
Regulation of GFAP expression in glial‐like cells of the rat pituitary intermediate lobe by lactation, salt‐loading, and adrenalectomy
Authors: Gary Keith A. , Chronwall Bibie M. 
Published: December 2004

AbstractGlial‐like cells in rat pituitary intermediate lobe were localized and characterized by immunohistochemistry with antisera against glial fibrillary acidic protein (GFAP) and S‐100. Individual GFAP immunoreactive (IR) cells possessed several processes that often branched into secondary and tertiary processes, terminating with end‐feet. The GFAP‐immunopositive cell population was distributed in specific rostrocaudal and dorsoventral patterns. The distribution and numbers of cells differed between male and female rats. Examination of altered physiological states, e.g., adrenalectomy, lactation, and salt‐loading, revealed state‐specific changes in the appearance and distribution of GFAP‐IR cells. Adrenalectomy and lactation increased GFAP‐IR glial‐like cell numbers, whereas salt‐loading decreased their numbers and the typical pattern of distribution. By contrast, S‐100–expressing cells were evenly distributed in male and female rats, and its expression was not affected by the experimental conditions. Double‐label immunocytochemistry indicated that GFAP‐IR cells are a subpopulation of S‐100‐IR cells. These results suggest that cells normally expressing only S‐100 may be induced to express GFAP under altered physiologic conditions. Copy 1995 Wiley‐Liss, Inc.
Effect of transforming growth factor‐β1 and ‐β2 on Schwann cell proliferation on neurites
Authors: Guénard Véronique , Rosenbaum Thorsten , Gwynn Lisa A. , Doetschman Thomas , Ratner Nancy , Wood Patrick M. 
Published: December 2004

AbstractMechanisms regulating Schwann cell proliferation during development are unclear. Schwann cell division is known to be driven by an unidentified mitogen present on the surface of axons, but it is not known whether other molecules play a role in regulating this proliferation. Transforming growth factor‐beta (TGF‐β) which is found in the developing peripheral nervous system (PNS) and is mitogenic for neuron‐free Schwann cells in vitro could be involved. We have investigated the effects of TGF‐β 1, TGF‐β 2 and antibodies to TGF‐β and TGF‐β 2 on axon driven Schwann cell proliferation. Rat embryonic dorsal root ganglion neurons (DRG) neurons and Schwann cells from the sciatic nerve were isolated, purified and recombined in vitro. Confirming earlier reports by others, we observed that TGF‐β 1 and TGF‐β 2 added to the culture medium stimulated the proliferation of Schwann cells in the absence of neurons. However, when added to neuron‐Schwann cell co‐cultures, TGFβ caused a variable response ranging from no effect to moderate inhibition of Schwann cell proliferation in different experiments. A stimulation of Schwann cell proliferation by TGFβ was never observed in neuron‐Schwann cell co‐cultures. Antibodies to TGF‐β and TGF‐β 2 did not influence axon driven Schwann cell proliferation. To further determine the role of TGF‐β in Schwann cell proliferation and myelination, we studied Schwann cell proliferation in cultures from mice in which the TGF‐β 1 gene was delected by homologous recombination. Neuron‐Schwann cell cultures from wild‐type, heterozygous and homozygous mice were used. No differences were observed in either Schwann cell proliferation or myelination between cultures obtained from homozygous mutants and their heterozygous and wild‐type controls. These findings suggest that TGF‐β does not function as a part of the mitogenic mechanism presented by neurons to Schwann cells, but that the presence of active TGFβ in the cellular environment might regulate the degree of proliferation induced by neuronal contact. Copy 1995 Wiley‐Liss, Inc.
Acidic pH rapidly increases immunoreactivity of glial fibrillary acidic protein in cultured astrocytes
Authors: Oh Tae H. , Markelonis George J. , Von Visger Jon R. , Baik Bonsook , Shipley Michael T. 
Published: December 2004

AbstractNeuroepithelial progenitor cells from forebrains of newborn rat pups develop into “mature” astrocytes in an epidermal growth factor‐containing medium free of serum (Von Visger et al: Exp Neurol 128:34, 1994). Eight‐week‐old “mature” astrocyte cultures on poly‐L‐lysine‐coated dishes were exposed to an acidic medium (pH 5.8–6.0) for 2–6 h. Immunoreactivity for glial fibrillary acidic protein (GFAP) dramatically and rapidly increased; this immediate increase was not affected by pretreatment with cycloheximide. In further experiments we found that the increase in GFAP was undiminished for 24–48 h after the acid‐treated astrocytes were returned to normal growth medium. The Ca2+ channel antagonists nifedipine and diltiazem attenuated the increase in GFAP immunoreactivity. These results suggest that extracellular acidosis may produce a rapid increase in GFAP immunoreactivity in astrocytes independent of de novo protein synthesis, possibly by increasing intracellular levels of free Ca2+ ions. Copy 1995 Wiley‐Liss, Inc.
The ependyma: A protective barrier between brain and cerebrospinal fluid
Authors: Del Bigio Marc R. 
Published: December 2004

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, Inc.
Calcium waves in dissociated retinal glial (Müller) cells are evoked by release of calcium from intracellular stores
Authors: Keirstead Susan A. , Miller Robert F. 
Published: December 2004

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 (Ambystoma tigrinum) 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+]i that 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+]i may 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+]i remain to be elucidated. © 1995 Wiley‐Liss, Inc.
Canine oligodendrocytes undergo morphological changes in response to basic fibroblast growth factor (bFGF) in vitro
Authors: Hoffman Kurt L. , Duncan Ian D. 
Published: December 2004

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, Inc.
AMPA‐type glutamate receptors in glial precursor cells of the rat corpus callosum: Ionic and pharmacological properties
Authors: Berger Thomas 
Published: December 2004

AbstractGlial cells in fiber tracts express various functional transmitter receptors, e.g., for glutamate. However, little is known about their biophysical and pharmacological profile. Using the in situ patch‐clamp technique, kainate‐ and AMPA‐induced conductance changes of glial precursor cells in the rat corpus callosum were investigated to study these aspects. Precursor cells were identified by their voltage‐gated currents and were easily discernable from astrocytes and oligodendrocytes. Kainate induced two overlying effects in these cells: the activation of a cationic current and the block of potassium conductances. Cesium in the pipette solution blocked potassium conductances nearly completely and the ionic profile of the kainate‐induced cationic current could be studied in detail. Full replacement of the sodium in the bath by calcium resulted only in a small kainate‐induced (calcium) inward current flow, but the kainate‐induced outward current carried by Cs+ was less affected reflecting a weak calcium permeability. The kainate response could be blocked by 6,7‐dinitroquinoxaline‐2,3‐dione (DNQX) and millimolar zinc concentrations. Co‐application of microinolar concentrations of zinc slightly enhanced the kainate‐induced current, while Evans Blue was without any significant effect. Cyclothiazide increased the kainate response by a factor of x6 while concanavalin A did not enlarge it. The AMPA‐induced current was amplified by a factor of X39 by cyclothiazide.The present data suggested the expression of weakly calcium‐permeable AMPA receptors on glial precursor cells in the rat corpus callosum. Only a small fraction of the agonist‐induced current could be seen without the appropriate blockers of receptor desensitization. An additional expression of kainate‐preferring glutamate receptors could not be shown. © 1995 Wiley‐Liss, Inc.
Amoeboid microglia expressing GD3 ganglioside are concentrated in regions of oligodendrogenesis during development of the rat corpus callosum
Authors: Ellison J. A. , de Vellis J. 
Published: December 2004

AbstractIn a recent study we demonstrated expression of the platelet‐derived growth factor α receptor (PDGFRα) in cells of the early oligodendrocyte lineage that were identified as either GD3 ganglioside + oligodendrocyte progenitors or O4 sulfatide + preoligodendrocytes. We also identified a subpopulation of GD3 immunoreactive cells that did not express mRNA for the PDGF receptor. The distinct large amoeboid morphology of these cells was characteristic of cells in the macrophage lineage rather than in the oligodendrocyte lineage. To determine if the GD3‐positive but PDGFRα mRNA‐negative cells were in the macrophage lineage, we compared the spatial and temporal expression patterns of GD3 ganglioside and ED1, a macrophage‐specific antigen. Analysis prenatally indicated that at embryonic day 15, ED1+ and GD3 + cell populations resided in the subpial connective tissue. At embryonic day 21, these two populations were seen in a region extending from the lateral ventricle through the subventricular and intermediate zones. In this study we report that these large, round, GD3 immunoreactive cells have the same cell morphology and anatomical distribution as the ED1 immunoreactive cells. Both cell populations contained pyknotic nuclei within their cytoplasm. Furthermore, the GD3+/PDGFRα‐ cells appear to be involved in clearing cellular debris in regions of gliogenesis. These data suggest that this subpopulation of GD3 immunoreactive cells belongs to the microglia/macrophage lineage. © 1995 Wiley‐Liss, Inc.
Long‐term production of neurotrophic factors by astrocyte cultures from hemiparkinsonian rat brain
Authors: Langan Thomas J. , Plunkett Robert J. , Asada Hideo , Kelly Kindra , Kaseloo Paul 
Published: December 2004

AbstractTransplantation of dopaminergic or neurotrophic tissues is an experimental treatment of Parkinson's Disease. However, in animal models sustained recovery may occur after surgical trauma to affected brain areas even in the absence of grafted tissue. Consequently, brain tissue reacting to local trauma in these experiments must be capable of substantial neurotrophic responses. To evaluate the potential of astrocytes in these neurotrophic responses, cultures were obtained from gelatin implants into striatal cavities that were created in hemiparkinsonian rats. The type 1 astrocyte phenotype as determined immunocytochemically was maximal at day 7 in vitro and paralleled the glial reaction in the adjacent brain parenchyma. Neurite‐promoting activity of the culture medium was determined in a chick dorsal root ganglion bioassay and also was established by 7 days. Nerve growth factor antibodies neutralized only around 40% of this activity. Neurotrophic activity was absent with assay of media from early or long‐term newborn rat astrocytes, and of medium conditioned by a monoyte/macrophage cell line. Passage after several months yielded astrocyte cultures that repeated a surge of neurite‐promoting activity. This long‐term potential to produce multiple neurotrophic factors indicates that autologous astrocytes in affected brain regions may serve either as targets for or agents of therapy of Parkinsonism. © 1995 Wiley‐Liss, Inc.
Biochemical subtypes of oligodendrocyte in the anterior medullary velum of the rat as revealed by the monoclonal antibody rip
Authors: Butt A. M. , Ibrahim M. , Ruge F. M. , Berry M. 
Published: December 2004

AbstractOligodendrocytes were studied in the anterior medullary velum (AMV) of the rat using the monoclonal antibody Rip, an oligodendrocyte marker of unknown function. Confocal microscopic imaging of double immunofluorescent labelling with antibodies to Rip and carbonic anhydrase II (CAII) revealed two biochemically and morphologically distinct populations of oligodendrocyte which were either Rip + CAII + or Rip + CAII−. Double immunofluorescent labelling with Rip and myelin basic protein (MBP) or glial fibrillary acidic protein (GFAP) provided direct evidence that Rip‐labelled cells were phenotypically oligodendrocytes and confirmed that Rip did not recognise astrocytes. Oligodendrocytes which were Rip+CAII+ supported numerous myelin sheaths for small diameter axons, whilst Rip+CAII− oligodendrocytes supported fewer myelin sheaths for large diameter axons. Morphologically, Rip+CAII+ oligodendrocytes corresponded to types I or II of classical nomenclature, whilst Rip+CAII− oligodendrocytes corresponded to types III and IV. The results demonstrated a biochemical difference between oligodendrocytes which myelinated small and large diameter fibres. © 1995 Wiley‐Liss, Inc.