bluuebunny/crossref_metadata_2025_split huggingface dataset:
Remyelination of demyelinated rat axons by transplanted mouse oligodendrocytes
Authors: Crang A. J. , Blakemore W. F. 
Published: January 2005

AbstractThe injection of the gliotoxic agent ethidium bromide (EB) into spinal white matter produces a CNS lesion in which it is possible to investigate the ability of transplanted glial cells to reconstruct a glial environment around demyelinated axons. This study demonstrates that transplanted mouse glial cells can repopulate EB lesions in rats provided tissue rejection is controlled. In X‐irradiated EB lesions in cyclosporin‐A‐treated rats, mouse oligodendrocytes remyelinated rat axons and, together with mouse astrocytes, re‐established a CNS environment. When transplanted into nonirradiated EB lesions in nude rats, mouse glial cells modulated the normal host repair by Schwann cells to remyelination by oligodendrocytes. In both X‐irradiated and non‐irradiated EB lesions, transplanted mouse glial cells behaved similarly to isogenic rat glial cell transplants (Blackemore and Crang Dev Neurosci, 1988;10:1–10; J Neurocytol, 1989;18:519–528). These findings indicate that the cell‐cell interactions involved in reconstruction of a glial environment are common to both mouse and rat.
Excitatory amino acid receptors in primary cultures of glial cells from the retina
Authors: María López‐Colomé Ana , Romo‐De‐Vivar Mónica 
Published: January 2005

AbstractBinding of 3H‐L‐aspartate to membranes from retinal glial cells in primary culture was characterized. Binding kinetics showed a saturable, reversible binding to three populations of sites with KB = 40,200, and 1,300 nM. The first two were present at 1 day in vitro (DIV), whereas the latter two were observed at 12 DIV. The possibility of the 40 nM site being neuronal cannot be discarded, since some neurons are present at 1 DIV. In 12 DIV cultures, the presence or absence of sodium determined two different pharmacological patterns, comparable to those described for electrogenic glutamate transport in Müller cells, and QA metabotropic receptors in astrocytes, respectively. Results suggest that, as has been shown for some receptors in nerve tissue, the properties of glial cell receptors undergo age‐dependent changes. In turn, this could be related to changes in the function of neurotransmitter substances during development.
High conductance anion channel in Schwann cell vesicles from rat spinal roots
Authors: Quasthoff Stefan , Strupp Michael , Grafe Peter 
Published: January 2005

AbstractPotassium uptake, possibly together with chloride, is one of the presumed functions of Schwann cells in the peripheral nervous system. However, the presence of chloride channels has not been demonstrated in adult Schwann cells. We present here a new method which allows single channel recordings to be made from Schwann cells in situ without enzymatic treatment. Isolated rat spinal roots were split mechanically into several bundles. Within about 30 min after this procedure small belb‐like vesicles (∼20–30 μm in diameter) with a clean surface appeared at the edges of the fibre bundles. Immunofluorescence microscopy with a surface marker for Schwann cell membranes (monoclonal antibody O4) revealed that the vesicles originate from Schwann cells. In standard patch clamp recordings with symmetrical bath and pipette solutions (excised inside‐out configuration) an anion channel with the following characteristics was mainly observed: (1) single channel slope conductance of 337 ± 5 pS in 125 mM KCl and 209 ± 6 pS in 125 mM K+ methylsulphate; (2) ion permeability ratio: PCl/PK/Pgluconate = 1/0.12/0.06; (3) linear current‐voltage relationship (range ± 60 mV) and (4) voltage‐ and time‐dependent inactivation (the channel was most active at potentials ± 20mV). Pharmacologically, the channel was completely blocked with zinc (1 mM) and barium (10 mM). A similar anion channel, showing characteristics 1 – (4), has been described in cultured Schwann cells of newborn rats (Gray et al., 1984). We now demonstrate that this channel is also present in adult Schwann cells in situ.
Amoeboid and ramified microglia: Their interrelationship and response to brain injury
Authors: Leong Seng‐Kee , Ling Eng‐Ang 
Published: January 2005

AbstractRio‐Hortega's hypothesis that transietly appearing amoeboid microglia might become ramified microglia in the adult and that the latter could differentiate into brain macrophages in the event of brain damage could not be proved because of inherent limitations in existing techniques. The present investigation used a novel method of labelling the rat supraventricular amoeboid microglia with an enduring fluorescet marker, rhodamine B isothiocyanate, introduced intraperitoneally. Observation of their subsequent development showed that they became transformed into the ramified microglia. Both te amoeboid and ramified microglia were OX‐42 positive, indicating their macrophage/monocyte lineage. Other microglia in the cerebral neocortex, which were also OX‐42 positive, were not derived from any of the rhodamine‐labelled cells. Rhodamine‐labelled cells, which were OX‐42 positive, appeared at all lesioned sites, and such were most likely blood derived monocytes. The antigeicity of the ramified microglia became elevated when rhodamine B isothiocyaate was present intracellularly and even more so with the presence of a earby intracerebral stab wound. © 1992 Wiley‐Liss, Inc.
Estradiol promotes cell shape changes and glial fibrillary acidic protein redistribution in hypothalamic astrocytes in vitro: A neuronal‐mediated effect
Authors: Torres‐Aleman Ignacio , Rejas Maria Teresa , Pons Sebastian , Garcia‐Segura Luis Miguel 
Published: January 2005

AbstractWe have previously shown that in hypothalamic mixed neuronal‐glial cultures both astrocytic shape and distribution of glial fibrillary acidic protein (GFAP) are modified by estradiol. In the present study, we have investigated whether or not the presence of neurons is necessary for these hormonal effects. In mixed neuronal‐glial hypothalamic cultures the proportion of process‐bearing GFAP‐immunoreactive cells was significantly increased after treatment for 30 min with 10−12 M 17β estradiol. This effect was present for at least 1 day and was reverted by incubating the cells in estradiol‐free medium. Estradiol incubation resulted in a progressive differentiation of GFAP‐immunoreactive cells from a flattened epithelioid morphology to bipolar, radial, and stellate shapes. This effect was not observed in pure hypothalamic glial cultures. Furthermore, incubation of hypothalamic glial cells with medium conditioned by estradiol‐treated mixed hypothalamic cultures did not affect the shape of GFAP‐immunoreactive astrocytes. In contrast, addition of hypothalamic neurons, but not cerebellar neurons or fibroblasts, to established hypothalamic glial cultures affected the development of estradiol sensitivity in astrocytes. These results indicate that estradiol induction of shape changes in hypothalamic astrocytes is not only dependent on the presence of hypothalamic neurons, but that physical contact between astrocytes and neurons is necessary for the manifestation of the effect of this hormone. © 1992 Wiley‐Liss, Inc.
The glial framework of central white matter tracts: Segmented rows of contiguous interfascicular oligodendrocytes and solitary astrocytes give rise to a continuous meshwork of transverse and longitudinal processes in the adult rat fimbria
Authors: Suzuki M. , Raisman G. 
Published: January 2005

AbstractThe cellular skeleton of the adult rat fimbria consists of regularly spaced interfascicular glial rows of considerable length, running in the longitudinal (axonal) axis of the tract.Each row consists of a series of repeated segments made up of a stretch of interfascicular oligodendrocytes lying in direct contact with each other, and separated from the adjacent segments by usually solitary interfascicular astrocytes. A typical segment would be around 60 μm long, and have an axial core of about eight contiguous oligodendrocytes surrounded by a shell of about 1,200 axons, 70% of which are myelinated. In the transverse plane of the tract, adjacent segments are stacked together with a core‐to‐core distance of around 15 μm.The interfascicular oligodendrocytes have radial stem processes (in a plane transverse to the axonal axis) which give rise to the longitudinal myelinating (internodal) processes. Both transverse and longitudinal oligodendrocytic processes are longer than the dimensions of the segment (in which their cell bodies lie) and its axonal shell. They thus cooperate in myelinating axons of adjacent segments in both planes.The interfascicular astrocytes have three distinct types of processes: radial, longitudinal, and vascular (bearing end feet). The radial astrocytic processes are thick and tapering, and the processes of individual astrocytes extend transversely (in the plane of the original embryonic radial glial processes) for a total of at least 100 μm. The considerably more numerous longitudinal astrocytic processes arise from all parts of the cell bodies and radial processes. They are up to at least 30 μm long, thin, untapering, and largely unbranched, and are interdigitated among the fimbrial axons.In the radial plane, the astrocytic radial processes spread out through a wide swathe of adjacent segments, so that the integrated meshwork of interpenetrating longitudinal processes arising from overlapping radial processes of astrocytes from many different interfascicular rows provides a continuous longitudinal substrate for the fimbrial axons. © 1992 Wiley‐Liss, Inc.
Effect of insulin of glucose and glycogen metabolism and leucine incorporation into protein in cultured mouse astrocytes
Authors: Kum W. , Zhu S. Q. , Ho S. K. S. , Young J. D. , Cockram C. S. 
Published: January 2005

AbstractInsulin, following binding to its receptor, produces a dose‐ and time‐dependent stimulation of entry of 2‐deoxy‐D‐[U‐14C] glucose and glycogen synthesis from D‐[U‐14C] glucose in cultured mouse astrocytes following differentiation. Maximal stimulation of both glucose entry (217% above basal) and of glycogen synthesis (209% above basal) was observed at an insulin concentration of 1.7 × 10−8 M. Insulin also stimulates the incorporation of leucine into astrocytic proteins with maximal stimulation (156% above basal) at an insulin concentration of 1.7 × 10−7 M, but no effect on leucine uptake was observed at an insulin concentration of 1.7 × 10−6 M. These results, together with a previous demonstration that insulin and certain insulin analogues stimulate pyrimidine nucleoside incorporation into nucleic acid, indicate that insulin has diverse actions on biomacromolecular metabolism in cultured mouse astrocytes. © 1992 Wiley‐Liss, Inc.
Migration of Schwann cells from the distal stump of the sciatic nerve 1 week after transection: The effects of insulin and cytosine arabinoside
Authors: Dubovy P. , Svizenska I. 
Published: January 2005

AbstractWe have examined the migratory capacity of Schwann cells from the distal stump of a 1‐week transected sciatic nerve of adult rat for a distance of 10 mm. The distal stump was introduced into the open end of a silicone chamber packed with artificial fibrin sponge (Gelaspon) soaked in phosphate‐buffered saline (control chambers), cytosine arabinoside (Ara‐C) (0.05 mM), or insulin (40 U/ml). Migrating Schwann cells were distinguished from fibroblasts by the presence of non‐specific cholinesterase (nChE) activity and glial fibrillary acidic protein (GFAP). The cells of distal stumps including Schwann cells accepted Gelaspon as a suitable adhesive substratum. In the chambers filled with Gelaspon soaked in phosphate‐buffered saline alone Schwann cells were outnumbered by fibroblasts. The addition of Ara‐C resulted in greater numbers of Schwann cells, which migrate longer distances into the chambers. The application of insulin enhanced Schwann cell migration as well. These morphologic observations were further supported by biochemical measurements of nChE activity. The results suggest an influence on Schwann cell migration by fibroblasts of connective tissue sheaths and a stimulation of Schwann cell migration by insulin. © 1992 Wiley‐Liss, Inc.
Microglia and cytokines in neurological disease, with special reference to AIDS and Alzheimer's disease
Authors: Dickson Dennis W. , Lee Sunhee C. , Mattiace Linda A. , Yen Shu‐Hui C. , Brosnan Celia 
Published: January 2005

AbstractMicroglia are associated with central nervous system (CNS) pathology of both Alzheimer's disease (AD) and the acquired immunodeficiency syndrome (AIDS). In AD, microglia, especially those associated with amyloid deposits, have a phenotype that is consistent with a state of activation, including immunoreactivity with antibodies to class II major histocompatibility antigens and to inflammatory cytokines (interleukin‐1‐β and tumor necrosis factor‐α). Evidence from other studies in rodents indicate that microglia can be activated by neuronal degeneration. These results suggest that microglial activation in AD may be secondary to neurodegeneration and that, once activated, microglia may participate in a local inflammatory cascade that promotes tissue damage and contributes to amyloid formation. In AIDS, microglia are the primary target of retroviral infection. Both ramified and ameboid microglia, in addition to multinucleated giant cells, are infected by the human immunodeficiency virus (HIV‐1). The mechanism of microglial infection is not known since microglia lack CD4, the HIV‐1 receptor. Microglia display high affinity receptors for immunoglobulins, which makes antibody‐mediated viral uptake a possible mechanism of infection. In AIDS, the extent of active viral infection and cytokine production may be critically dependent upon other factors, such as the presence of coinfecting agents. In the latter circumstance, very severe CNS pathology may emerge, including necrotizing lesions. In other circumstances, HIV infection microglia probably leads to CNS pathology by indirect mechanisms, including release of viral proteins (gp120) and toxic cytokines. Such a mechanism is the best hypothesis for the pathogenesis of vacuolar myelopathy in adults and the diffuse gliosis that characterizes pediatric AIDS, in which very little viral antigen can be detected.
Microglia in degenerative neurological disease
Authors: McGeer Patrick L. , Kawamata Toshio , Walker Douglas G. , Akiyama Haruhiko , Tooyama Ikuo , McGeer Edith G. 
Published: January 2005

AbstractMicroglia express many leukocyte surface antigens which are upregulated in such chronic degenerative neurological diseases as Alzheimer's disease (AD) and amyotrophic lateral sclerosis (ALS). These surface antigens include leukocyte common antigen, immunoglobulin Fc receptors, MHC class I and class II glycoproteins, β2‐integrins, and the vitronectin receptor. Ligands for these receptors are also found. They include immunoglobulins, complement proteins of the classical pathway, T lymphocytes of the cytotoxic/suppressor and helper/inducer classes, and vitronectin. T lymphocytes marginate along capillary venules, with some penetrating into the tissue matrix. Immunoglobulins and complement proteins are synthesized locally in brain, although they may also come from the bloodstream if the blood‐brain barrier is compromised. The membrane attack complex, which is formed from C5b‐9, the terminal components of complement, has been identified in AD and multiple sclerosis brain tissue. In addition, proteins designed to defend against bystander lysis caused by the membrane attack complex, including protectin, C8 binding protein, clusterin, and vitronectin, are associated with damaged neuronal processes in AD. Autodestruction may play a prominent part in these 2 diseases.
Characterization of “plasma proteins” secreted by cultured rat macroglial cells
Authors: Zahs Kathleen R. , Bigornia Violeta , Deschepper Christian F. 
Published: January 2005

AbstractThe brain is isolated behind a blood‐tissue barrier that restricts the access of circulating proteins to neural cells. There is evidence that some of these proteins are synthesized within the central nervous system. The present study examines the synthesis and secretion of such proteins by cultured macroglial cells. Primary glial cultures were derived from cortical and subcortical regions of neonatal rat brains, and subsequent secondary cultures were enriched in type‐1 astrocytes, type‐2 astrocytes, or oligodendrocytes. Newly synthesized proteins were immunoprecipitated from the culture media using antisera directed against whole rat serum. All three types of glial cells secreted a range of plasma proteins. In general, type‐1 astrocytes secreted more of these proteins than did type‐2 astrocytes or oligodendrocytes, although the one‐dimensional polyacrylamide gel electrophoresis (PAGE) profiles were specific for each cell type. Antisera directed against specific plasma proteins identified three of the most abundant proteins secreted by type‐1 astrocytes as transferrin, α‐2‐macroglobulin, and ceruloplasmin. Northern blot analysis of cellular RNA confirmed that type‐1 astrocytes contained transferrin mRNA, and that it was more abundant in cultures derived from subcortical regions than from cortical regions. In situ hybridization studies revealed that virtually all type‐1 and type‐2 astrocytes contained transferrin mRNA.Since the proteins identified in this study have been proposed to have a variety of neurotrophic roles in the central nervous system, these data further extend the range of possible functions that glial cells may serve in the CNS.
Stimulation of astrocyte proliferation by purine and pyrimidine nucleotides and nucleosides
Authors: Christjanson Lisa J. , Middlemiss Pamela J. , Rathbone Michel P. 
Published: January 2005

AbstractProliferation of brain astrocytes as a result of cell death has been well documented in vivo. Dying cells release purine and pyrimidine nucleosides and nucle‐otides and their deoxy derivatives both from soluble intracellular pools and from DNA and RNA. Previously, we have observed that purine nucleosides and nucleotides stimulate chick astrocyte proliferation in vitro. To further our analysis, we questioned whether pyrimidines or the deoxy derivatives of purine nucleosides and nucleotides might also be astrocyte mitogens. Pyrimidine nucleosides, nucleotides, and their deoxynucleotide derivatives were uniformly inactive. In contrast, deoxyguanosine, deoxyadenosine, and their mono‐, di‐, and triphosphates stimulated thymidine incorporation into astrocytes at concentrations similar to those at which their ribonucleoside and ribonucleotide analogues were active. Inosine, IMP, ITP, and hypoxanthine were active, whereas xanthine and xanthosine were not. However, XMP, XDP, and XTP stimulated thymidine incorporation. The effects of the nucleosides and deoxynucleosides were inhibited by antagonists of adenosine A2 receptors. These data indicate that most purine nucleosides, deoxynucleosides, and their 5′ mono, di‐, and triphosphate derivatives released from damaged cells are capable of stimulating astrocyte proliferation in vitro and may contribute to astrocyte proliferation in vivo following injury to the CNS.
Purinergic P2Y receptors on astrocytes are directly coupled to phospholipase A2
Authors: Bruner Gretchen , Murphy Sean 
Published: January 2005

AbstractATP stimulates arachidonic acid mobilization and eicosanoid production in cultured astrocytes via P2Y‐purinergic receptors. To assist in determining the mechanism of phospholipase A2 activation and the role of calcium in eicosanoid production, cultures were pretreated with pertussis toxin (PTx). ATP‐evoked eicosanoid release was inhibited by PTx in a concentration‐dependent fashion. Inositol phospholipid hydrolysis was partially attenuated by PTx, but the concentrations required were approximately 50 times greater than those for inhibition of eicosanoid production, suggesting that phospholipase C activation is not necessary for eicosanoid synthesis. Stimulation of eicosanoid release by other P2Y‐purinergic receptor agonists was also inhibited by PTx; however, PTx had no effect on eicosanoid release evoked by ionomycin or thapsigargin, nor did it affect ATP‐stimulated calcium influx or mobilization from intracellular stores. Increases in intracellular free calcium concentration alone were insufficient to stimulate eicosanoid production, but maximal production was dependent upon the concentration of extracellular calcium. These results suggest that the P2Y‐purinergic receptor is coupled to phospholipase A2 via a guanine nucleotide‐binding protein, and that extracellular calcium may also be involved in the synthesis of eicosanoids by astrocytes.
Distribution of metallothionein in the human central nervous system
Authors: Blaauwgeers H. G. T. , Smitt P. A. E. Sillevis , De Jong J. M. B. V. , Troost D. 
Published: January 2005

AbstractThe distribution of metallothionein (MT), a metal‐binding protein, was examined immunohistochemically in the normal human brain and spinal cord. Paraffinembedded brain tissue from three patients who had died from a non‐neurological disease and were free of histopathological central nervous system alterations were processed. The results of the present study demonstrate that MT is readily detectable in a subgroup of astrocytes in the normal human brain. MT staining is most intense on grey matter astrocytes that bear short stout processes and which probably represent protoplasmic astrocytes.Using anti‐MT and anti‐glial fibrillary acidic protein immunostaining, we could demonstrate two subpopulations of astrocytes that were mutually exclusive. The functional significance of MT‐expression in protoplasmic astrocytes is not entirely clear. Metal detoxification is only one of the many postulated functions of MT. The finding that staining for MT permits subtyping of astrocytes may be of great importance in glia research and surgical pathology of the human brain. © 1993 Wiley‐Liss, Inc.