bluuebunny/crossref_metadata_2025_split huggingface dataset:
Acylation of lysophosphatidylcholine by brain membranes
Authors: Premkumar N. , Sun G. Y. , Macquarrie R. A. 
Published: January 2005

AbstractBrain microsomes catalyze the acylation of lysophosphatidylcholine (lysoPtdCho) in the presence and absence of added CoA derivatives. The catalytic activity is distributed widely in various subcellular fractions from rat or bovine cerebral cortex as measured by the conversion of 1‐[14C] palmitoyl‐sn‐glycero‐3‐phosphocholine to [14C]PtdCho. Analysis of this latter compound revealed that the dipalmitoyl derivative is the predominant molecular species, which is formed in this reaction by transacylation between two [14C]lysoPtdCho molecules. This lysoPtdCho: lysoPtdCho transacylation reaction was enhanced several‐fold by the addition of oleoyl‐CoA, which also is an effective donor of acyl groups in the acyl‐CoA: lysoPtdCho acyltransferase‐catalyzed reaction. Measurements of the initial velocity of the transacylation reaction were used to determine kinetic constants. Apparent Km values for lysoPtdCho in the presence and absence of oleoyl‐CoA were 29 μM and 104 μM, respectively, and the corresponding maximal velocities were 0.11 and 1.06 nmol min−1 mg−1, respectively. Oleoyl‐CoA at 4 μM produced half‐maximal stimulation of the transacylation reaction. CoA also stimulated the rate of conversion of [14C]lysoPtdCho to [14C]PtdCho, either in the presence or absence of oleoyl‐CoA, with a half‐maximal effect of CoA at 80 μM. These results may be important in understanding the regulation of PtdCho synthesis and the mechanism by which acyl group composition of this compound is controlled. © 1993 Wiley‐Liss, Inc.
Influence of janusin and tenascin on growth cone behavior in vitro
Authors: Taylor J. , Pesheva P. , Schachner M. 
Published: January 2005

AbstractJanusin and tenascin are glia‐derived, structurally related, extracellular matrix glycoproteins of the J1 family that are expressed in vivo at times and in locations where active neurite outgrowth occurs, but also when the formation or stabilization of cytoarchitectonic boundaries appears to be in operation. To resolve this apparent functional dichotomy, we have studied the behavioral response of growth cones, growing in culture on the permissive substrate laminin, to janusin and tenascin, by video time lapse microscopy. When janusin and tenascin were offered as sharp substrate boundaries, dorsal root ganglion (DRG) and retinal ganglion neuron growth cones avoided growing on these molecules, but were not induced to collapse. On the other hand, when janusin and tenascin were offered, in a mixture with laminin, as uniform substrates, DRG growth cones displayed a collapsed morphology and were able to advance at a faster rate than on laminin alone. In contrast, the outgrowth of retinal ganglion neuron growth cones was completely inhibited under these conditions, underscoring a cell type specificity in the response of growth cones to these molecules. Using several monoclonal antibodies binding to distinct epitopes on the tenascin molecule, we have identified two domains responsible for growth cone repulsion, on epidermal growth factor (EGF)‐like repeats 3‐5 and fibronectin type III homologous repeats 4 and 5. These domains are different from the one previously recognized to be involved in neurite outgrowth on a uniform tenascin substrate. We conclude that both molecules may promote or retard growth cone advance, depending on the spatial expression pattern and the neuronal cell type. © 1993 Wiley‐Liss, Inc.
Prednisolone enhances myogenesis and dystrophin‐related protein in skeletal muscle cell cultures from mdx mouse
Authors: Passaquin A. C. , Metzinger L. , Léger J. J. , Warter J.‐M. , Poindron P. 
Published: January 2005

AbstractThe differentiation of skeletal muscle cells from mdx mice which lack dystrophin expression was examined after glucocorticoid treatment, namely α‐methylprednisolone (PDN). Primary skeletal muscle cell cultures were established from newborn mdx, congenic C57BL/10, and allogenic BALB/C mice. We show that PDN promotes the myogenesis of both mdx‐ and control mice‐derived cultures as determined by (1) the number of myotubes, (2) acetylcholine receptors, and (3) dystrophin and dystrophin‐related protein levels. These results support the hypothesis that PDN could enhance the myogenesis of satellite cells and increase dystrophin‐related protein expression in DMD treated patients. © 1993 Wiley‐Liss, Inc.
Evidence for activation of astrocytes via reactive microglial cells following hypoglossal nerve transection
Authors: Svensson M. , Eriksson N. P. , Aldskogius H. 
Published: January 2005

AbstractFollowing peripheral nerve injury, resident microglial cells proliferate and astrocytes undergo hypertrophy, as evidenced, e.g., by an increase in the levels of glial fibrillary acidic protein (GFAP). In a previous study we have shown that infusion of cytosine arabinoside (ARA‐C) into the rat brain blocks the axotomy‐induced proliferation of microglial cells. This experimental approach has been used in the present study in order to explore the issue of whether the reactive microglial cells are mediators of the increased GFAP expression in the hypoglossal nucleus of the rat following axotomy. Quantitative analysis of sections processed for immunocytochemistry or in situ hybridization demonstrated a marked increase in GFAP‐like immunoreactivity and GFAP‐mRNA, respectively, in the ipsilateral hypoglossal nucleus 4 and 7 days after axotomy in control experiments. These increases failed to occur in axotomized animals treated with ARA‐C. Therefore, our data are compatible with the hypothesis that activation of astrocytes following axotomy as measured by increased expression of GFAP and its mRNA is induced secondarily to the microglial response. © 1993 Wiley‐Liss, Inc.
Phagocytosis of myelin by microglia in vitro
Authors: Smith M. E. 
Published: January 2005

AbstractPrevious experiments from this laboratory have shown that peritoneal macrophages in culture will phagocytize myelin. Myelin preopsonized with myelin antibodies is phagocytized to a much greater extent than untreated myelin, indicating that macrophages ingest myelin by an Fc receptor. The present work was undertaken to determine the characteristics of myelin phagocytosis by microglia, the resident macrophages of the central nervous system. Microglia isolated from 4–5 day primary cultures of newborn rat brains were shown to bind and phagocytize myelin labeled in the lipids by 14C‐acetate. Both binding and phagocytosis as shown by the appearance of 14C‐cholesterol ester were greatly increased if labeled myelin was preopsonized with antiserum to myelin basic protein or galactocerebroside. Both preopsonized and untreated myelin were phagocytized more actively by microglia than by peritoneal macrophages under the same culture conditions. Microglia cultured in the presence of GM‐CSF showed slightly increased cholesterol ester production from opsonized myelin, but the effect of GM‐CSF was significantly greater than myelin pretreated with control serum (34% increase) or untreated myelin (154% increase). There was no significant effect of GM‐CSF on myelin phagocytosis by peritoneal macrophages. Cerebrospinal fluid containing immunoglobulin drawn from rabbits with acute EAE also opsonized myelin to increase phago cytosis by microglia, as has been previously shown with peritoneal macrophages. These results indicate that microglia may actively participate in myelin destruction in demyelinating diseases where myelin antibodies or a source of GM‐CSF may be present. © 1993 Wiley‐Liss, Inc.This article is a US Government work and, as such, is in the public domain in the United States of America.
Protein kinase C‐ε is a developmentally regulated, neuronal isoform in the chick embryo central nervous system
Authors: Mangoura D. , Sogos V. , Dawson G. 
Published: January 2005

AbstractProtein kinase C (PKC) is expressed as many isoforms and in high quantities in the central nervous system (CNS), which suggests an important role for this enzyme in neuronal development and function. We used specific antibodies to investigate the expression of the known PKC isoforms in extracts from chick major CNS areas during embryogenesis, from day 3 (E3) of incubation to day 1 post‐hatching (P1). PKC‐ε was the predominant isoform and was expressed from E6 onward in all brain regions, except retina (E12 and on). PKC‐α/β and ‐ζ isoforms were expressed at lower levels prior to PKC‐ε expression and throughout embryogenesis. No other isoforms were detected in neural tissue preparations. We then used neural culture systems derived from the chick CNS to study the expression of PKC isoforms in neuroblasts, cortical neurons, and cortical glial cells. Western blotting and immunostaining of neuroblastenriched cultures, derived from E3 CNS, showed only the Ca2+‐dependent PKC‐α/β to be present. Studies on neuronal cultures derived from E6 cerebral hemispheres revealed only the Ca2+‐independent PKC‐ε to be expressed in neurons, as predicted by the developmental studies on tissue homogenates. PKC‐ε immunoreactivity was seen intracellularly in differentiating neurons, regardless of their neurotransmitter phenotypes, and it correlated well with the level of neuronal activity. Furthermore, PKC‐α/β immunoreactivity was verified on glia cells, as the glial lineage emerges in E15 cortical cultures. These data suggest that PKC‐ε expression is associated with the final neuroblast division in neurons, and the correlation of PKC isoform expression and neural cell lineage is discussed. © 1993 Wiley‐Liss, Inc.
Retinoic acid responsive gene product, midkine, has neurotrophic functions for mouse spinal cord and dorsal root ganglion neurons in culture
Authors: Michikawa M. , Kikuchi S. , Muramatsu H. , Muramatsu T. , Kim S. U. 
Published: January 2005

AbstractMidkine (MK) is the product of a retinoic acid responsive gene and is a member of a new family of heparin‐binding growth factors. Neurotrophic effects of MK were examined using cultured spinal cord and dorsal root ganglion (DRG) neurons derived from fetal mouse. MK, which was added to the culture medium at concentrations of 1–100 ng/ml, promoted survival of both types of neurons approximately 5‐fold after 7 days in culture. For spinal cord neurons, the increased survival was reflected in an increase of choline acetyltransferase activity. MK also promoted neurite extension in spinal cord (2‐fold) and DRG (1.7‐fold) neurons. The survival‐promoting activity of MK to these neurons was comparable to that of basic fibroblast growth factor (bFGF) and leukemia inhibitory factor (LIF). In spite of its significant effects on fetal neurons, MK was ineffective in sustaining survival of DRG neurons derived from postnatal mice. From these results, we conclude that MK is a neurotrophic factor to embryonic spinal cord and DRG neurons, and we propose that MK plays a significant role in embryogenesis of the nervous system. © 1993 Wiley‐Liss, Inc.
Effect of vitamin D Deficiency and 1,25‐dihydroxyvitamin D3 on metabolism and D‐glucose transport in rat cerebral cortex
Authors: Stio M. , Lunghi B. , Lantomasi T. , Vincenzini M. T. , Treves C. 
Published: January 2005

AbstractWe previously demonstrated that feeding rats Steenbock and Black's rickets‐inducing diet produces remarkable changes in the metabolic pattern of the in testinal mucosa, kidney, and liver and in some membrane transport Systems of intestinal mucosa and kidney. 1,25‐Dihydroxyvitamin D3 administration to rachitic rats did not always prove to be effective in restoring normal values.We have now investigated the effect of 1,25‐dihydroxyvitamin D3 on the levels of some metabolites in rat cerebral cortex, on the activity of some enzymes, and on the transport of 2‐deoxy‐D‐glucose and D‐glucose in synaptosomes. Our experiments were carried out on three rat groups: control, rachitic, and rachitic treated with 1,25‐dihydroxyvitamin D3. The decrease in phosphorus content and the increase in citrate concentration observed in rachitic rat cerebral cortex were corrected by 1,25‐dihydroxyvitamin D3 treatment.The activity of acetylcholinesterase, glucose‐6‐phosphate dehydrogenase, and acyl phosphatase significantly increased in rachitic rat synaptosomes, as well as NAD+‐dependent isocitrate dehydrogenase in cerebral cortex mitochondria; the administration of 1,25‐dihydroxyvitamin D3 to rachitic rats restored enzyme levels to normal. The transport of 2‐deoxy‐D‐glucose and D‐glucose in rachitic rat synaptosomes was lower than in the control group and returned to control values in consequence of 1,25‐dihydroxyvitamin D3 treatment.The results reported here support the hypothesis of a participation of 1,25‐dihydroxyvitamin D3 in some aspects of cerebral cortex metabolism.
Endogenous peptide Tyr‐Pro‐Trp‐Gly‐NH2 (Tyr‐W‐MIF‐1) is transported from the brain to the blood by peptide transport system‐1
Authors: Banks W. A. , Kastin A. J. , Ehrensing C. A. 
Published: January 2005

AbstractTyr‐W‐MIF‐1 (Tyr‐Pro‐Trp‐Gly‐NH2) is a recently isolated peptide that belongs to a larger family that includes Tyr‐MIF‐1 (Tyr‐Pro‐Leu‐Gly‐NH2) and MIF‐1 (Pro‐Leu‐Gly‐NH2). Despite similarities in structure, Tyr‐MIF‐1 and MIF‐1 can act differently in behavioral, blood‐brain barrier (BBB) transport, and receptor binding Systems. Tyr‐W‐MIF‐1, like Tyr‐MIF‐1, has both Opiate and antiopiate activity, but may be more opiate‐like than Tyr‐MIF‐1. TyrMIF‐1, but not MIF‐1, is transported from brain to blood by peptide transport system (PTS)‐1. PTS‐1 transports mainly Tyr‐MIF‐1 and methionine enkephalin, but does not transport amino acids, peptide fragments of Tyr‐MIF‐1, D‐Tyr‐MIF‐1, or unrelated peptides and proteins. We tested whether Tyr‐WMIF‐1 also was transported across the BBB and, if so, whether PTS‐1 was involved. 125I‐Tyr‐W‐MIF‐1 had a half‐time disappearance from the brain of 22.4 min. This is faster than the efflux occurring with nonsaturable reabsorption ofthe cerebrospinal fluid and, therefore, is consistent with saturable transport, but it is slower than the efflux rate of Tyr‐MIF‐1, suggesting a less robust transport than for Tyr‐MIF‐1. Self‐inhibition with excess unlabeled Tyr‐W‐MIF‐1 confirmed a saturable component, with a dose of 4.2 nmol producing 50% inhibition. Competition studies between radioactively labeled Tyr‐W‐MIF‐1 and unlabeled Tyr‐MIF‐1 and between labeled Tyr‐MIF‐1 and unlabeled Tyr‐W‐MIF‐1 showed that Tyr‐WMIF‐1 is transported by PTS‐1 with Tyr‐MIF‐1 being the preferred ligand. Aluminum and serotonergic agents modulate PTS‐1 activity and they affected Tyr‐W‐MIF‐1 transport in a manner consistent with its mediation through PTS‐1. It is concluded that Tyr‐W‐MIF‐1 is transported out of the brain by a saturable system that is probably PTS‐1, although transport is less robust than that of Tyr‐MIF‐1. © 1993 Wiley‐Liss, Inc.This article is a US Government work and, as such, is in the public domain in the United States of America.
Serotonin‐containing terminals synapse on septohippocampal neurons in the rat
Authors: Milner T. A. , Veznedaroglu E. 
Published: January 2005

AbstractSerotonin [5‐hydroxytryptamine (5‐HT)] is thought to be involved in mnemonic functions and dysfunctions possibly by directly contacting neurons in the medicl septal and diagonal band nuclei (i.e., the septal complex) that project to the hippocampal formation. However, there is no cellular substrate for this modulation. Thus, we examined the ultrastructure and synaptic association of 5‐HT‐containing terminals in relation to septohippocampal neurons in the septal complex of the rat brain. Projection neurons were identified by retrograde transport of wheat germ agglutinated apo‐horseradish perodidase conjugated to colloidal gold particles (WANG) following an injection into the ventral hippocampal formation of uneashetized adult rats. After a 1 day survival, setions through the septal complex were labeled with antibodies to 5‐HT immunoreactivity (5‐HT‐I) were observed in close proximity to neurons containing retogardely transported WAHG. By electron microscopy, 5‐HT‐I immunoreacitity (5‐HT‐I) were observed in close proximity to neurons containing retrogadely transported WAHG. By electron microscopy, 5‐HT‐I was found exclusively in axons and axon terminals. Axons were primarily unmyelinated. Terminals with 5‐HT‐I were 0.35–1.2 μm in diameter and contained numerous small, clear vesicles and 0–4 large, dense‐core vesicles. The 5‐HT‐labeled terminals: (1) contacted perikarya and dendrites (220 of 349); (2) were closely apposed to other terminals (25 of 349); or (3) had no neuronal contacts in the plane of section analyzed (104 of 349). The 5‐HT‐labeled terminals formed exclusively symmetric synases on perikarya; some of these perikarya as well as some large dendrites similarly contacted by the 5‐HT‐labeled terminals also contained WAHG affiliated with lysosomes and multivesicular and “sequestration” bodies in the cytoplasm. However, the majority of terminals with 5‐HT‐I formed contacts on the shafts of small unlabeled dendrites (69% of 220); most of these were characterized as either asymmetric synapses or appositions not separated by astrocytes in the plane of section analyzed. We conclude that 5‐HT‐containing terminals in the rat septal complex: (1) directly modulate septohippocampal and other neurons through symmetric (potentially inhibitory) synapses on soma and proximal dendrites; and (2) form primarily asymmetric (potentially excitatory) synapses with distal (small) dendrites from neurons of unidentified origin. These findings suggest that serotonin may affect learning and memory through modulation of septal efferents to the hippocampal formation and may have direct relevance to the neuropathological basis for Alzheimer's disease. © 1993 Wiley‐Liss, Inc.
Analysis of the human MBP promoter in primary cultures of oligodendrocytes: Positive and negative cis‐acting elements in the proximal MBP promoter mediate oligodendrocyte‐specific expression of MBP
Authors: Wrabetz L. , Shumas S. , Grinspan J. , Feltri M. L. , Bozyczko D. , McMorris F. A. , Pleasure D. , Kamholz J. 
Published: January 2005

AbstractSince the regulation of myelin basic protein expression depends primarily on the initiation of transcription, we analyzed the 5′ flanking region of the human myelin basic protein gene in transient transfection studies in primary cultures of developing oligodendrocytes. We demonstrated that 149 base pairs 5′ of the initiation of transcription was sufficient to direct oligodendrocyte‐specific expression of myelin basic protein. The capsite of the fusion transcript was identical with that of the endogenous myelin basic protein transcript, and chloramphenicol acetyl transferase reporter gene expression was restricted to oligodendrocytes in these cultures. Within this 149 base pair region, one distal, negative cis‐acting segment, containing a consensus nuclear factor I site, and one proximal, positive cis‐acting segment were identified. The distal segment behaved more negatively in Cos‐7 cells than in oligodendrocytes, reducing expression to background levels. Furthermore, these functionally important cis‐acting segments bound oligodendrocyte nuclear proteins in a pattern differing from other cells, including Cos‐7 cells. Interestingly, the distal segment increased heterologous SV40 promoter activity in oligodendrocytes but had no effect on the SV40 promoter in Cos‐7 cells. We conclude that the functionally negative distal segment may mediate oligodendrocyte‐specific expression of MBP by restricting its expression in other cells. These experiments strongly support using primary cultures of oligodendrocytes for analyzing the myelin‐specific promoters. © 1993 Wiley‐Liss, Inc.
Platelet‐activating factor is a messenger in the electroconvulsive shock‐induced transcriptional activation of c‐fos and zif‐268 in hippocampus
Authors: Marcheselli V. L. , Bazan N. G. 
Published: January 2005

AbstractPlatelet‐activating factor (PAF, 1‐O‐alkyl‐2‐acetyl‐sn‐glycero‐3‐phosphocholine), undetectable in resting neural tissue, accumulates in brain during seizures. A hetrazepine, BN‐50730, is shown here to displace [3H]PAF‐specific binding from microsomal, but not from synaptosomal membranes, indicating selectivity for a high affinity intracellular binding site. Rats pretreated with BN‐50730 by intraperitoneal or intracerebroventricular injection exhibited an inhibition of the electroconvulsive shock (ECS)‐induced expression of c‐fos and zif‐268 in hippocampus. A much more pronounced, dose‐dependent inhibition of ECS‐induced zif‐268 mRNA in hippocampus by intracerebroventricular injection of of BN‐50730 was observed. It is concluded that, in the hippocampus, PAF IS A MEDIATOR OF THE EXPRESSION OF zif‐268 and, to a lesser extent, c‐fos through an intracellular specific binding site. Thus, PAF may be a messenger in signal regulated zinc‐finger transcription factors, and in other immediate‐early genes involved in long‐term synaptic plasticity changes. © 1994 Wiley‐Liss, Inc.
The long‐term down‐regulation of dihydropyridine receptors by bay K 8644 in PC12 cells
Authors: Nikodijevic B. , Nikodijevic‐Kedeva D. , Oshima M. , Paige B. , Guroff G. 
Published: January 2005

AbstractTreatment of PC12 cells with Bay K 8644 for 12 hr or more leads to an almost 80% decrease in the subsequent ability of Bay K 8644 to stimulate the uptake of radioactive calcium into the cells. This effect is a property of the s(−)isomer of Bay K 8644; pre‐treatment with the R(+)isomer, now known to be a calcium channel blocker, has the opposite effect. This treatment is specific in that is does not intergfere with the stimulation of calcium uptake by potassium, ATP, or nerve growth factor. Such treatment is accompanied by a 90% decrease in the ability of Bay K 8644 to stimulate the release of norepinephrine. The characteristics of the binding of [3H]isradipine to control and to treated cells indicates that the decrease in the effect of dihydropyridines is accompanied by a marked decrease in the number of dihydropyridine binding sites with no apparent change in the affinity of the remaining sites. The continued ability of depolarizing levels of potassium to stimualte calcium uptake and the induction of the protooncogene c‐fos in Bay K 8644‐treated cells indicates that the L‐type calcium channels are still intact, but are simply unresponsive to dihydropyridine agonists. © 1994 Wiley‐Liss, Inc.This article is a US Government work and, as such, is in the public domain in the United States of America.