bluuebunny/crossref_metadata_2025_split huggingface dataset:
Glial response to dorsal root lesion in the irradiated spinal cord
Authors: Sims T. J. , Gilmore S. A. 
Published: May 2005

AbstractExposure of the rat lumbar spinal cord to X‐rays during the early postnatal period results in a marked reduction in the glial populations within the irradiated region. The present study was undertaken to determine what effects this reduction of glia, particularly astrocytes, has on the pattern and characteristics of the scar formation that follows root injury in the normal spinal cord. Morphological assessments 60 days following injury of the right L4 dorsal root revealed a distinct difference in the extent of the astrocyte response between the irradiated and the nonirradiated rats. In the nonirradiated animals, a thick astrocytic scar composed of multiple layers of astrocyte processes formed over the dorsal horn and adjacent portions of the dorsal surface of the cord. This astrocytic response was not confined to the surface of the spinal cord but extended also into the root, i.e., into regions normally considered as PNS. In irradiated rats, the astrocytes did not form a thick scar nor did they extend into the injured root. Instead, they formed a glia limitans and were at most only one or two layers thick over the region of cord comparable to that occupied by the thick astrocytic scar in the nonirradiated rats. Mechanisms involved in the glial response of the irradiated spinal cord to dorsal root injury are discussed, particularly with regard to the possible positive effect that this reduction in scar formation may have on regrowth of injured dorsal root axons into the spinal cord environment. © 1992 Wiley‐Liss, Inc.
Expression of adrenergic receptors in individual astrocytes and motor neurons isolated from the adult rat brain
Authors: Shao Yanping , Sutin Jerome 
Published: May 2005

AbstractAttempts to show the distribution of adrenergic receptors (ARs) in autoradiographs of a brainstem motor nucleus following elimination of motor neurons yielded the unexpected result of an increase in β‐AR density. This increase was related to the gliosis accompanying the motor neuron degeneration. To determine the cells on which the AR subtypes were located, we dissociated cells from various regions of the adult rat brain and subsequently identified astrocytes by glial fibrillary acidic protein (GFAP) immunofluorescence. Slides containing the astrocytes were prepared for autoradiography using the nonselective β ligand 125I‐iodocyanopindolol (125ICYP) or the α1 ligand 125IBE 2254 (125I‐HEAT). The addition of the selective β1 blocker betaxolol or the β2 blocker ICI 118.551 to the incubation medium to displace 125ICYP binding was used to determine the binding of β‐AR subtypes.The great majority (> 88%) of isolated astrocytes sampled from the trigeminal motor nucleus, cerebral cortex, striatum, and cerebellum showed β‐AR binding. Astrocytes from the first three regions had similar average densities of β‐ARs, whereas the density in cerebellar astrocytes was 2‐ to 3‐fold greater. The β2‐AR subtypes was proportionally greater than the β1 subtype in each region. Reactive astrocytes isolated from the trigeminal motor nucleus after degeneration of motor neurons showed a β‐AR density nearly 2‐fold greater than resting astrocytes from the same region, with the β1 subtype showing the greater proportional increase. There was no β‐AR binding on trigeminal motor neurons.Astrocytes also showed a significant level of α1‐AR binding. No differences in α1‐AR binding were found in normal astrocytes isolated from the different regions, nor was there an increase in reactive astrocytes. In contrast, trigeminal motor neurons had an α1‐AR density nearly 10 times greater than astrocytes.In terms of the NE modulation of synaptic responses in motor neurons, the distribution of ARs would permit NE to act indirectly through α1 and β receptors on astrocytes and directly through α1 receptors on motor neurons. © 1992 Wiley‐Liss, Inc.
Calcium dependence of serotonin‐evoked conductance in C6 glioma cells
Authors: Manor David , Moran Nava , Segal Menahem 
Published: May 2005

AbstractWhole‐cell membrane currents and imaging of intracellular calcium concentrations ([Ca2+]i) were used to investigate the role of calcium in a response to serotonin of C6 glioma cells. Activation of a high‐affinity serotoinin receptor induced a transient rise in calcium concentration in these cells and activated a predominantly potassium conductance, with a small chloride component. Perfusion of the cytoplasm with an internal solution containing high calcium concentration induced similar but prolonged increase of membrane conductance. The responsiveness of C6 cells to serotonin was negatively correlated with the concentration of the unbound calcium chelator BAPTA when BAPTA‐buffered calcium‐containing intracellular solutions were used. Responses to serotonin persisted in the absence of external calcium, decreased gradually, and then recovered partially after replenishment of extracellular calcium. These findings substantiate the direct role of intracellular calcium in mediating the serotonin response, and indicate that serotonin‐induced release of calcium from intracellular stores is sufficient for the activation of conductance in the C6 glioma cell line. © 1992 Wiley‐Liss, Inc.
Postnatal development of dye‐coupling among astrocytes in rat visual cortex
Authors: Binmöller F.‐J. , Müller C. M. 
Published: May 2005

AbstractIntercellular coupling among astrocytes was studied in rat visual cortex slices from animals aged 1 week to 4 months. Cell coupling via gap junctions was determined by the dye spread of the low molecular weight dye Lucifer Yellow CH injected into electrophysiologically identified cells to adjacent cells. Coupling among glial cells was first detected at postnatal day 11 and was thereafter consistently observed until adulthood. Dye spread was observed up to 300 μm radially from the injected cell covering multiple cortical layers. Following dye injection into a single cell up to several hundred Lucifer Yellow‐positive cells could be observed. Quantitative analysis revealed a similar extent of dye spread at different developmental stages including a quite constant number of dye‐coupled astrocytes from the end of the second postnatal week to adulthood. Double labelling of Lucifer Yellow‐filled cells with an antiserum against the glial fibrillary acidic protein confirmed the astrocytic nature of the injected and coupled cells. Comparison of the density of dye‐coupled cells in a given area and the total number of astrocytes as revealed by immunocytochemical staining suggests that dye‐coupling includes the entire local astrocytic population. It is concluded that coupling among astrocytes via gap junctions in rat visual cortex occurs shortly after birth and reflects one of the first steps in astroglial maturation. © 1992 Wiley‐Liss, Inc.
Immuno‐electron microscopical localization of vimentin and glial fibrillary acidic protein in mouse astrocytes and their precursor cells in culture
Authors: Abd‐El‐Basset Ebtesam M. , Ahmed Ijaz , Kalnins Vitauts I. , Fedoroff Sergey 
Published: May 2005

AbstractImmuno‐electron microscopy was used to localize the distribution of vimentin and glial fibrillary acidic protein (GFAP) in mouse astrocytes and their precursor cells in primary cultures. In astroblasts and astrocytes, vimentin and GFAP form intermediate filaments (IF), which are heteropolymers, as previously observed in gliomas. Astrocytes and their precursor cells may have IF composed of GFAP‐vimentin heteropolymer or vimentin alone, but IF composed of GFAP only were not seen. It seems that the formation of IF that are GFAP‐vimentin heteropolymers is a feature of normal astroglia development and that the ratio of GFAP to vimentin in these IF reflects the degree of differentiation and functional state of the cell. © 1992 Wiley‐Liss, Inc.
Differential migration of astrocytes grafted into the developing rat brain
Authors: Hatton James D. , Nguyen Mindie H. , Sang U Hoi 
Published: May 2005

AbstractFetal and neonatal astrocytes migrate in specific patterns when transplanted into the adult rat host brain. However, it is unclear whether these astrocytes demonstrate the same degree of mobility during early brain development. In the present study, neonatal cortical, hippocampal, and hypothalamic astrocytes were collected from the brains of 1‐ to 3‐day‐old rats and placed in tissue culture. After 14 to 21 days, cultures enriched in astrocytes were harvested and labelled with either the fluorescent dye Fast Blue or fluorescein‐labelled latex beads. They were then transplanted into the right frontal cerebrum of neonatal rats at 2,5,8, and 11 days postpartum. Seven days after transplantation, animals were sacrificed and their brains were fixed by immersion in aldehydes, sectioned on a cryostat, and examined with fluorescence microscopy. Transplanted astrocytes migrated along the corpus callosum, internal capsule, glial limitans, ventricular linings, and hippocampal structure. Labelled cells were also found in the contralateral hemisphere in day 2 brains. Migration in a radial fashion from the injection site toward the periphery was a particularly obvious pattern, and was most pronounced in these younger hosts. In days 5 and 8 rat brains, astrocyte migration became more restricted to the hemisphere of implantation. In 11‐day‐old host brains hemispheric restriction and other region‐specific influences became manifest and specifically modulated migration. Radial migration was absent in the 11‐day‐old host group except for cells of cortical origin. The observed results demonstrate that neonatal cortical, hippocampal, and hypothalamic astrocytes transplanted into the neonatal cerebrum migrate in patterns that are more extensive than in the adult brain. This suggests that cellular migration in the neonatal brain is governed by factors that are less restrictive than those regulating migration in the adult brain. In particulur, our observations imply that radial glia may provide migratory substrates for transplanted astrocytes, and region‐specific regulation of migration may begin around 11 days after birth. © 1993 Wiley‐Liss, Inc.
Excitatory amino acid‐induced phosphoinositide hydrolysis in Müller glia
Authors: López‐Colomé Ana María , Ortega Arturo , Romo‐De‐Vivar Mónica 
Published: May 2005

AbstractThe presence of excitatory amino acid (EAA) receptors coupled to phosphoinositide metabolism in primary cultures of Müller (glial) cells from the chick retina was established. The order of potency of analogues for stimulating [3H]inositol phosphate (IP) accumulation was quisqualate (QA) > L‐glutamate (L‐Glu) = kainate (KA) > N‐methyl‐D‐aspartate (NMDA) > L‐aspartate (L‐Asp) with EC50 in the range of 1‐100 μM. 1‐Aminocyclopentane‐1,3‐dicarboxylate (trans‐ACPD), α‐amino‐3‐hydroxy‐5‐methyl‐4‐isox‐azolepropionate (AMPA), 2‐amino‐3‐phosphonopropionate (AP3), and 2‐amino‐4‐phosphonobutyrate (AP4) showed no effect either on basal concentration or on stimulated accumulation of [3H]IPs. The effect of EAA was potently inhibited by the ionotropic NMDA receptor antagonists 2‐amino‐5‐phosphonopentanoate (AP5), 3‐[(RS)‐2‐carboxy‐piperazin‐4‐yl]‐propyl‐1‐phosphonate (CPP), and (+)‐5‐methyl‐10,11‐dihydro‐5H‐diben‐zo[a,d]cyclohepten‐5‐10‐imine (MK‐801); L‐Glu antagonists at non‐NMDA receptors, the quinoxalines NBQX and DNQX, inhibited weakly the response to L‐Glu, KA, and NMDA, and more potently that to QA. The translocation of protein kinase C was also stimulated by EAA with the same pharmacological profile, and was partially inhibited by kynurenate (KYN). L‐Glu and KA induced 45Ca2+ influx, which was decreased by KYN and CNQX. EAA‐induced [3H]IPs accumulation was decreased by verapamil but not by nifedipine, and slightly diminished by dantrolene. Results demonstrate that EAA‐induced phosphoi‐nositide hydrolysis in Müller cells shows pharmacological differences with that in astrocytes and neuronal cells and could be triggered by a different mechanism. © 1993 Wiley‐Liss, Inc.
Oligodendrocyte development and differentiation in the rumpshaker mutation
Authors: Fanarraga M. L. , Sommer I. U. , Griffiths I. R. , Montague P. , Groome N. P. , Nave K.‐A. , Schneider A. , Brophy P. J. , Kennedy P. G. E. 
Published: May 2005

AbstractThe jimpy rumpshaker (jprsh) mutation is an amino acid substitution in exon 4 (Ile186→Thr) of the proteolipid protein (PLP) gene on the X chromosome. Affected mice show moderate hypomyelination of the central nervous system (CNS) with increased numbers of oligodendrocytes in the white matter of the spinal cord, a feature distinguishing them from other PLP mutations such as jp, in which premature cell death occurs with reduced numbers of oligodendrocytes. Myelin sheaths of jprsh immunostain for myelin basic protein (MBP) and DM‐20, but very few contain PLP. This study examines the differentiation of oligodendrocytes cultured from the spinal cords of young mutant and wild type mice using various surface and cytoplasmic antigenic markers to define the stage of development. The majority of oligodendrocytes from mutant mice progress normally to express MBP; approximately 30%, relative to wild type, contain DM‐20 at the in vivo age of 16 days, but very few immunostain for PLP or the O10 and O11 markers. The morphology of mutant cells in respect to membrane sheets and processes appears similar to normal. The jprsh oligodendrocyte is, therefore, characterized by a failure to express the markers indicative of the most mature cell; however, it is probably able to achieve a normal period of survival. These data, taken in conjunction with previous results, suggest that the PLP gene has at least two functions; one, probably involving PLP, is concerned with a structural role in normal myelin compaction; the other, perhaps related to DM‐20 (or another lower molecular weight proteolipid), is essential for cell survival. The mutation in jprsh at residue 186 suggests that this region, which is common to PLP and DM‐20, is not critical for this latter function. © 1993 Wiley‐Liss, Inc.
Endogenous opioid systems and the growth of oligodendrocyte progenitors: Paradoxical increases in oligodendrogenesis as an indirect mechanism of opioid action
Authors: Hauser Kurt F. , Gurwell Julie A. , Bhat Narayan R. 
Published: May 2005

AbstractEndogenous opioids inhibit nervous system development by inhibiting the proliferation of certain neuronal and glial progenitors. To determine whether opioids affect the growth of preoligodendrocytes, the effects of the endogenous opioid [Met5]‐enkephalin were examined in preoligodendrocytes in primary mixed‐glial and preoligodendrocyte‐enriched (>98% pure) cultures. Proliferating preoligodendrocytes in mixedglial or preoligodendrocyte‐enriched cultures were continuously treated for a total of 40 h with either basal growth media (controls), 1 μM [Met5]‐enkephalin, 1 μM [Met5]‐enkephalin plus the opioid antagonist naloxone (3 μM), or naloxone alone (3 μM), and incubated in [3H]‐thymidine (0.2 μCi/ml/4–6 h) after 34–36 h of opioid exposure. Opioid dependent changes in DNA synthesis were assessed autoradiographically in O4‐immunoreactive oligodendrocyte progenitors. Naloxone alone significantly decreased the rate of DNA synthesis and number of O4‐immunoreactive preoligodendrocytes in mixed‐glial cultures. However, naloxone and/or [Met5]‐enkephalin did not affect DNA synthesis or the number of O4‐immunoreactive preoligodendrocytes in cultures enriched in preoligodendrocytes. The results suggest that astrocytes, or perhaps another cell type, play a permissive role in opioid‐dependent alterations in preoligodendrocyte proliferation. Endogenous opioids affect the genesis of neural cells by both direct and indirect mechanisms. © 1993 Wiley‐Liss, Inc.
Synaptic transmission in the hippocampus: Critical role for glial cells
Authors: Keyser David O. , Pellmar Terry C. 
Published: May 2005

AbstractThe importance of glial cells in controlling the neuronal microenvironment has been increasingly recognized. We now demonstrate that glial cells play an integral role in hippocampal synaptic transmission by using the glial‐specific metabolic blocker fluoroacetate (FAC) to selectively inhibit glial cell function. FAC inhibits evoked intracellular postsynaptic potentials (PSPs; IC50 = 39 μM) as well as population PSPs (IC50 = 65 μM) in field CA1 of the guinea pig hippocampal slice. Spontaneous synaptic transmission is concurrently decreased. These effects are time and dose dependent. ATP concentrations in glial but not neuronal elements are also significantly reduced with FAC treatment. Simultaneous application of the metabolic substrate isocitrate with FAC prevents both the reduction in glial ATP concentrations and the decrease in evoked PSPs. Given that isocitrate is selectively taken up by glia, these data further support a glial specific metabolic action of FAC. Additionally, FAC has no postsynaptic effects as peak responses to iontophoretically applied glutamate are unchanged. However, the decay of both iontophoretic and evoked PSPs are prolonged following FAC treatment suggesting inhibition of glutamate uptake may contribute to the FAC‐induced depression of synaptic potentials. These results show, for the first time, that glial cells are critical for maintenance of synaptic transmission and suggest a role for glial cells in the modulation of synaptic efficacy. © 1994 Wiley‐Liss, Inc.
GD3+ cells in the adult rat optic nerve are ramified microglia rather than 0–2Aadult progenitor cells
Authors: Wolswijk Guus 
Published: May 2005

AbstractThe adult central nervous system (CNS) contains a population of adult oligodendrocyte‐type‐2 astrocyte (O‐2A) progenitor cells (O‐2Aadult progenitor cells). These cells may provide a source of the new oligodendrocytes that are needed to repair demyelinated lesions. In order to examine the role of O‐2Aadult progenitor cells in the regeneration of the oligodendrocyte population following demyelinating damage, it is essential to be able to identify such cells unambiguously in sections of adult CNS tissue. The present study examined whether antibodies to the ganglioside GD3 specifically label O‐2Aadult progenitor cells in cultures and sections of adult optic nerve, since previous studies on the developing CNS had suggested that O‐2Aperinatal progenitor cells were GD3+ in vitro and in vivo. Evidence is presented indicating that, although O‐2Aadult progenitor cells in vitro were labelled with the R24 mAb (an anti‐GD3 mAb), all GD3+ cells in sections of adult optic nerve bound the OX‐42 mAb and the B4 isolectin derived from Griffonia Simplicifolia, and thus were not O‐2Aadult progenitor cells, but ramified microglia. The data suggest that O‐2Aadult progenitor cells become GD3+ when placed in culture and that ramified microglia lose GD3‐expression in vitro. © 1994 Wiley‐Liss, Inc.
A physiological measure of carbonic anhydrase in müller cells
Authors: Newman Eric A. 
Published: May 2005

AbstractCarbonic anhydrase activity was characterized in freshly dissociated Müller cells of the salamander retina. Intracellular pH was monitored using ratio imaging of the indicator dye BCECF as extracellular Pco2 was varied. The extracellular solution was switched rapidly (141 ms rise time) from a HEPES buffered to a CO2‐HCO−3 buffered solution (both pH 7.4). Introduction of CO2‐HCO−3 produced a rapid cell acidification. Cell pH dropped from a steady‐state pH of 7.02 in HEPES solution to pH 6.81 in CO2‐HCO−3. Methazolamide, a carbonic anhydrase inhibitor, dramatically reduced the initial rate of acidification, demonstrating that the acidification was produced by the carbonic anhydrase‐catalyzed hydration of CO2. The initial rate of acidification, 52.6 pH units per min (0.88 pH units per s), was reduced ∼ 150‐fold to 0.36 pH units per min by 10−3 M methazolamide. Half‐maximal inhibition occurred at a methazolamide concentration of 5.6. 10−7 M. The carbonic anhydrase inhibitor acetazolamide (10−3 M) also greatly reduced the rate of cell acidification. The latency to the onset of carbonic anhydrase inhibition was 660 ms for methazolamide and 7.5 s for acetazolamide. The carbonic anhydrase inhibitor benzolamide (10−4 M, 4 min exposure), which is poorly membrane permeant, had little effect on the rate of cell acidification, indicating that the site of carbonic anhydrase action was intracellular. The activity of Müller cell carbonic anhydrase may help to buffer extracellular CO2 variations in the retina. © 1994 Wiley‐Liss, Inc.
Stimulation of in vitro myelin synthesis by microglia
Authors: Hamilton Steven P. , Rome Leonard H. 
Published: May 2005

AbstractCentral nervous system myelin is elaborated by oligodendrocytes, which have been studied extensively in cell culture. Dissociated brain cultures allow in vitro analysis of events in myelinogenesis, including cell‐cell interactions. Microglia, the primary phagocytic cell of the central nervous system, appear in developing fiber tracts prior to the onset of myelination in vivo. To gain insight into potential oligodendrocytemicroglial interactions during development, these cells were co‐cultured and various parameters of myelin synthesis were measured. In co‐culture, microglia stimulated the synthesis of sulfatide, a myelin‐specific galactolipid, in oligodendrocytes, as well as the expression of the myelin‐specific proteins myelin basic protein and proteolipid protein. Activity of the oligodendrocyte cytoplasm‐specific enzyme 2′,3′‐cyclic nucleotide 3′‐phosphohydrolase was not elevated, suggesting that the effects of microglia were not due to stimulation of oligodendrocyte proliferation. This was confirmed by the inability of microglia to induce significant DNA synthesis. Conditioned medium from cultured microglia provided a similar stimulatory activity, suggesting that the increase in myelin synthesis does not require contact between oligodendrocytes and microglia. These findings suggest a stimulatory role for microglia during myelinogenesis. © 1994 Wiley‐Liss, Inc.