bluuebunny/crossref_metadata_2025_split huggingface dataset:
Glial processes, identified through their glial‐specific 130 kD surface glycoprotein, are juxtaposed to sites of neurogenesis in the leech germinal plate
Authors: Cole Robert N. , Morell Robert J. , Zipser Birgit 
Published: January 2005

AbstractGlial processes, bearing a unique 130 kD surface protein, are located at key sites of morphogenic movement and neuronal differentiation in the leech germinal plate. A midline glial fascicle resides at the primary axis of embryonic symmetry, alongside which teloblasts move as they generate their bandlets of stem cells. The n‐bandlets straddle the midline glia and are known to produce most of the central neuroblasts. The midline glia then defasciculates as neuroblasts begin to aggregate into neuromers. The defasciculated processes expand into these neuromeres, molding the future central neuropile. Neuroblasts will initiate primary axons toward the midline glia. As the neuromeres mature, midline glial process thin out to demarcate the orientation of the future connectives, which are the major longitudinal axon tracts along the midline. Next, segmental but still primordial glia appear in the neuromeres. Initially, they also project longitudinally, then transversely, demarcating the other two major axonal pathways–the central commissures and peripheral roots. Finally, macroglial processes proliferate as massive axon growth invades the central and peripheral nervous system. Thus, glial processes with different developmental histories accompany different aspects of leech neurogenesis. In other systems, glia have been shown to promote the differentiation and the guidance of neurons. It remains to be seen whether the glial‐specific 130 kD protein is a receptor mediating these typical glial functions in the leech germinal plate.
Caprine β‐mannosidosis: Development of glial and myelin abnormalities in optic nerve and corpus callosum
Authors: Lovell Kathryn L. 
Published: January 2005

AbstractIn caprine β‐mannosidosis, an inherited dysmyelinating disorder, the myelin deficit shows substantial variation throughout the nervous system. In this study morphometric analysis of optic nerve and corpus callosum sections at selected developmental stages was conducted in order to investigate development and persistence of myelin sheaths, the population of axons ensheathed, and the extent of myelin deficits and glial cell abnormalities. The results show that the myelin deficit is severe at very early stages of development and persists to about the same extent into postnatal life. The corpus callosum, much more severely involved than the optic nerve, contains a substantially smaller percentage of myelinated axons when compared to control. In both regions, larger axons are preferentially myelinated. In the corpus callosum before myelination begins, many glial cells appear abnormal, suggesting an early cellular defect. In the postnatal, myelin‐deficient corpus callosum, there is a substantial decrease in glial cell density as compared to control, with abnormal appearance of many of the remaining cell profiles. These results define developmental characteristics of the dysmyelination in caprine β‐mannosidosis and document both the early appearance and the persistence of glial cell body and myelin abnormalities.
Serum influences the differentiation of membrane structure in cultured astrocytes
Authors: Landis Dennis M. D. , Weinstein Lori A. , Skordeles Christine J. 
Published: January 2005

AbstractThe membranes of mammalian astrocytic processes apposed to blood vessels or forming the surface of the brain contain high concentrations of a characteristic intramembrane particle aggregate, termed “assemblies.” In order to identify developmental processes which contribute to this remarkable regional specialization of membrane structure, we have devised culture conditions which support the differentiation of assemblies in secondary cultures of astrocytes derived from neonatal rat forebrain. We report here that different lots of fetal calf serum vary dramatically in their capacity to support the differentiation of assemblies. Fetal calf serum thus appears to exert two distinct influences on astrocyte development: it promotes the differentiation of type 2 astrocytes from bipotential precursor cells, as shown by others, and it influences the density of assemblies in type 1, flat, GFAP‐immunoreactive astrocytes in our secondary cultures. Horse serum and defined media also support the appearance of assemblies in flat, GFAP‐immunoreactive astrocytes. The separate effects of serum supplementation upon cell lineage and membrane differentiation have to be carefully considered in studies designed to examine factors influencing astrocytic development in vitro.
Developing forebrain astrocytes are sensitive to thyroid hormone
Authors: Gould Elizabeth , Frankfurt Maya , Westlind‐Danielsson Anita , McEwen Bruce S. 
Published: January 2005

AbstractPrevious studies have shown that developing neurons of the basal forebrain and hippocampus are sensitive to thyroid hormone (Gould and Butcher: J. Neurosci., 9:3347–3358, 1989; Rami et al: Neuroscience, 19:1217–1226, 1986). In order to determine whether or not thyroid hormone influences the development of astrocytes in brain regions where neurons are affected, we performed vimentin and glial fibrillary acidic protein (GFAP) immunocytochemical and single‐section Golgi‐impregnation analyses on the basal forebrain and hippocampus of control and neonatally thyroid hormone treated rats. For purposes of comparison, glial cells of the pontomesencephalotegmental (PMT) region, a region where developing neurons are not morphologically affected by thyroid hormone imbalances (Gould and Butcher, op. cit.), were also examined. Neonatal thyroid hormone treatment resulted in a premature disappearance of vimentin‐immunoreactive radial glia in the basal forebrain and hippocampus. In addition, a premature appearance of GFAP‐immunoreactive astrocytes with mature morphological characteristics was observed in the basal forebrain and hippocampus of thyroid hormone treated animals. Quantitative analyses revealed significant increases in the density of GFAP‐immunostained astrocytes and in the cross‐sectional cell body area and the number of primary processes in Golgi‐impregnated astrocytes of the basal forebrain and hippocampus of animals treated neonatally with thyroid hormone. In contrast, no changes in any of these parameters were observed in glial cells of the PMT region with neonatal thyroid hormone treatment.
Morphological changes of astroglia in the cerebellar cortex of developing mice after neonatal administration of cytosine arabinoside
Authors: Ono Katsuhiko , Mizukawa Kiminao , Yanagihara Mamoru , Tokunaga Akira 
Published: January 2005

AbstractNeonatal administration of cytosine arabinoside (Ara‐C) induced marked hypoplasia of the mouse cerebellum. In 17–20‐day‐old mice with neonatal Ara‐C injections, the external granular layer was still preserved as an irregular cell laminae in the superficial part of the cerebellum, in contrast to its complete disappearance in normal animals at these stages. Immunohistochemical examination using anti‐glial fibrillary acidic protein and monoclonal antibody‐1D11 (Ono et al: Dev. Brain Res., 50:154–159, 1989) demonstrated malformation of a palisade‐like arrangement of labeled glial fibers in the superficial part of the Ara‐C treated mouse cerebellum. Furthermore, the immunoreactive astroglia were observed just beneath the pial membrane and their processes were oriented to the deeper part of the molecular layer.
Glial influences on axonal growth in the primary olfactory system
Authors: Doucette R. 
Published: January 2005

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 agents.
Effect of exogenous fatty acids on lipid synthesis, marker‐enzymes, and development of glial cells maintained in serum‐free culture
Authors: Sykes Jane E. C. , Lopes‐Cardozo Matthijs 
Published: January 2005

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 oligodendrocytes in the culture system used.
Reactive astrogliosis after basic fibroblast growth factor (bFGF) injection in injured neonatal rat brain
Authors: Eclancher Francoise , Perraud Frederic , Faltin Jan , Labourdette Gerard , Sensenbrenner Monique 
Published: January 2005

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 injury.
Ultrastructural identification of HRP‐injected oligodendrocytes in the intact rat optic nerve
Authors: Ransom Bruce R. , Butt Arthur M. , Black Joel A. 
Published: January 2005

AbstractGlial cells in the rat optic nerve were visualized by intracellular injections of horseradish peroxidase (HRP). A novel class of cell was encountered that was presumed to be an oligodendrocyte on the basis of arguments related to its light microscopic appearance after intracellular staining (Butt and Ransom, Glia 1989; 2:470–475). These cells had 10–20 parallel processes 200–300 μm long that were oriented exclusively along the long axis of the optic nerve; the parallel processes were connected to the cell body by thin branches 15–30 μm long. To determine if these HRP‐filled cells were oligodendrocytes, they were examined ultrastructurally; all cells examined in this way were unequivocally found to be myelin‐producing oligodendrocytes. The oligodendrocytes contained intracellular organelles that were characteristic of this cell type, including abundant Golgi profiles and microtubules. In addition, HRP was found to fill the inner and outer tongue processes of myelin sheaths and the paranodal loops at nodes of Ranvier, proving that the entire cytoplasmic border surrounding the myelin sheath rapidly communicates by intracellular diffusion with the cell body. This electron microscopic study demonstrates that oligodendrocytes in the rat optic nerve can be positively identified by their distinctive light microscopic appearance after intracellular dye injection, and provides light microscopic criteria for establishing the number, distribution, and dimensions of the myelin segments provided by individual oligodendrocytes.
Tracing glial cell lineages in the mammalian forebrain
Authors: Goldman James E. , Vaysse Pierre J.‐J. 
Published: January 2005

AbstractAstrocytes and oligodendrocytes emerge in late gestational and early post‐natal development in the mammalian CNS. The nature, and number, of progenitors for each glial type is a central question. This review will focus upon several unresolved issues relating to glial cell lineages and describe new methods to try to illuminate these issues further: (1) How can developmental patterns by which immature neuroectodermal cells give rise to classes of neurons and glia be understood in the context of lineage? (2) What are the lineage relationships among the various cell classes, how many glial lineages are there in the developing CNS, and how can recent methods of clonal analysis using stable markers be used to clarify lineage patterns? (3) Do patterns of gliogenesis vary in different regions of the CNS? (4) How do patterns of gliogenesis observed in vitro relate to those in vivo?.
Cell origin and identity in Limb regeneration and development
Authors: Ferretti Patrizia , Brockes Jeremy P. 
Published: January 2005

AbstractThe occurrence of limb regeneration in adult urodele amphibians raises fundamental questions about the relationship between development and regeneration. The use of monoclonal antibodies as cell markers has provided clear evidence that blastemal cells, the progenitor cells of the regenerate, are not the same as limb bud cells in the embryo. For one of these antibodies the distinction has been traced to the relationship between limb regeneration and the nerve supply. Innervation of the limb bud during development appears to establish nerve‐dependent growth control for regeneration. The cell markers have also contributed to the problem of how the blastemal cells arise after amputation, although several important questions remain to be answered.
Ion channels in cultured adult human schwann cells
Authors: McLarnon James G. , Kim Seung U. 
Published: January 2005

AbstractSingle channel currents have been recorded from cultured adult human Schwann cells. In both cell‐attached and ‐excised (inside‐out) patches, openings from a high‐conductance (360 pS) channel were observed; measurements of the zero‐current potential indicated that the channel was predominantly selective for chloride. Depolarizing and hyperpolarizing voltage steps activated the anion channel, which subsequently reverted to a closed state even in the presence of the maintained step. A second channel, with a conductance near 20 pS and with a current amplitude that increased with patch hyperpolarization, passed inward K+ currents in both cell‐attached and inside‐out patches. The mean open times for this channel were near 20 ms at the cell resting potential and decreased with patch hyperpolarization. The presence of these anion and cation selective channels in the human Schwann cell membrane would be consistent with a role for the cells in the regulation of extracellular K+.
Isolated growth cones stimulate proliferation of cultured Schwann cells
Authors: Dent Erik W. , Ida James A. , Yoshino Jun E. 
Published: January 2005

AbstractA growth cone‐enriched fraction was prepared from 3–4 day rat cerebra. Examination of the growth cone fraction by electron microscopy revealed numerous structures circular in appearance that contain a number of features common to neuronal growth cones in vivo. The isolated growth cones stimulated a dose‐dependent incorporation of [3H]‐thymidine into cultured Schwann cells in a manner similar to that observed with an axolemma‐enriched fraction prepared from adult rat brainstem. The mitogenic activities of both the growth cone fraction and axolemma‐enriched fraction were decreased 50% and 20%, respectively, by treatment with heparitinase I. The mitogen for Schwann cells present in the isolated growth cones appears to be similar to that found in axolemma‐enriched fractions prepared from adult rats.
Activation of endothelin receptors by sarafotoxin regulates Ca2+ homeostasis in cerebellar astrocytes
Authors: Holzwarth James A. , Glaum Steven R. , Miller Richard J. 
Published: January 2005

AbstractWe carried out experiments designed to investigate the effects of sarafotoxin‐6B (SFTx) on [Ca2+]i in cerebellar astrocytes using the Ca2+ indicator fura‐2. Both endothelin‐1 and sarafotoxin‐6B increased [Ca2+]i in individual cerebellar astrocytes in cell culture. The shape of the response was variable but usually consisted of an initial peak of [Ca2+]i followed by an extended plateau increase in [Ca2+]i. In Ca2+‐free medium only the initial peak was observed. If Ca2+ was subsequently readmitted to the external medium a plateau was now formed. When external Ca2+ was removed during a plateau, [Ca2+]i rapidly declined; replacing the external Ca2+ reversed this decline. The plateau was also reversibly reduced by addition of Ni2+ (5 mM) to the external medium. Addition of 50 mM K+ produced a small increase in [Ca2+]i in most cells. This response was blocked by nimodipine. However, nimodipine only slightly blocked the plateau increase in [Ca2+]i that was formed following activation of endothelin receptors. Furthermore, perfusion of cells with 50 mM K+ during the plateau portion of a response to SFTx reduced [Ca2+]i. In some cells addition of a phorbol ester produced a sustained increase in [Ca2+]i that was blocked by nimodipine. In conclusion, activation of endothelin receptors by SFTx in cerebellar astrocytes produces both Ca2+ mobilization and Ca2+ influx. The pathway for Ca2+ influx is predominantly a non‐voltage‐dependent one, although some entry through a dihydropyridine‐sensitive pathway also appears to occur. Furthermore, activation of protein kinase C in cerebellar astrocytes activates voltage‐sensitive Ca2+ channels. © 1992 Wiley‐Liss, Inc.
Protein kinase C isoforms in human glioblastoma cells
Authors: Misra‐Press Anita , Fields Alan P. , Samols David , Goldthwait David A. 
Published: January 2005

AbstractProtein kinase C (PKC), an enzyme involved in signal transduction, responds to diacyl glycerol and also to phorbol ester, a ligand analogous to diacyl glycerol. We have studied the expression of the major isoforms (α, βI, βII, and γ) in eight human glioblastoma cell lines. In all eight lines, PKC‐α mRNA and protein were expressed. In none of the eight did a probe for PKC‐βI and ‐βII mRNA give positive results nor were Western blots for PKC‐βII positive. The half‐life for PKC α mRNA was approximately 16 h and levels of the mRNA were increased slightly following addition of phorbol myristate acetate (PMA) or transforming growth factor‐beta (TGFβ). PKC‐γ was present in most of the glioblastomas. In cell line A172, 82% of the PKC‐α was present in the cytosol with the remainder evenly divided between plasma membrane and nucleus. Thirty minutes after addition of PMA, 33% of the total original protein was in the plasma membrane and 48% in the nuclear fraction. By 21 h, no PKC‐α was recovered from any fraction. PKC‐γ was also down‐regulated in the presence of PMA, but there was no evidence for translocation to the plasma membrane or nuclear fraction. In a more detailed study, translocation of PKC‐α in the presence of PMA was complete by 10 min, and a major decrease in the PKC translocated to the plasma‐membrane fraction occurred some time between 2 and 4 h after PMA addition, while a major decrease in the translocated nuclear fraction occurred some time after 6 h. cAMP alone had no effect on the PKC α protein level or distribution, nor did it alter the translocation and down‐regulation due to PMA exposure. In these studies the level of PKC‐α mRNA in tumors was similar to that in normal glial cells. © 1992 Wiley‐Liss, Inc.
Interleukin‐1β regulates proenkephalin gene expression in astrocytes cultured from rat cortex
Authors: Negro Alessandro , Tavella Adriana , Facci Laura , Callegaro Lanfranco , Skaper Stephen D. 
Published: January 2005

AbstractGlial cells execute essential functions in central nervous system (CNS) development and are also believed to play important roles during gliosis in response to trauma or disease. These developmental and pathological states have also been associated with elevated expression of opioid genes. Because levels of the cytokine interleukin‐1β (IL‐1β) increase following CNS lesions, we examined the possible influence of IL‐1β on the expression of opioid genes in astrocytes cultured from rat cortex. Proenkephalin mRNA expression was stimulated by IL‐1β in a time‐ and concentration‐dependent manner, being maximal with 5 U/ml IL‐1β at 4h. Although the β‐adrenergic agonist isoproternol was also active, interferon, glutamate, and carbacol were not. Unlike isoproterenol, the actions of IL‐1β were not associated with a cyclic adenosine monophosphate (AMP)‐dependent pathway. Interleukin‐1β also regulated a proenkephalin‐chloramphenicol acetyltransferase fusion gene transiently transfected into astrocytes, with a dose‐response similar to that active in proenkephalin mRNA. These effects of IL‐1β were region‐specific, not being observed with either cerebellar or hippocampal astrocytes; however, isoproterenol was active in the latter cell populations. Proenkephalin mRNA in cortical astrocytes was stimulated following a temperature stress. These results suggest that enhanced proenkephalin gene expression in astrocytes by IL‐1β may be important in neuroimmune interactions and in trauma‐induced CNS injury or stress. © 1992 Wiley‐Liss, Inc.