bluuebunny/crossref_metadata_2025_split huggingface dataset:
Myelin basic protein content of aggregating rat brain cell cultures treated with cytokines and/or demyelinating antibody: Effects of macrophage enrichment
Authors: Loughlin A. J. , Woodroofe M. N. , Cuzner M. L. , Honegger P. , Comte V. , Matthieu J. ‐M. 
Published: January 2005

AbstractThe demyelinative potential of the cytokines interleukin‐1α (IL‐1α), interferon‐γ (IFN‐γ), and tumor necrosis factor‐α (TNF‐α) has been investigated in myelinating aggregate brain cell cultures. Treatment of myelinated cultures with these cytokines resulted in a reduction in myelin basic protein (MBP) content. This effect was additively increased by anti‐myelin/oligodendrocyte glycoprotein (α‐MOG) in the presence of complement. Qualitative immunocytochemistry demonstrated that peritoneal macrophages, added to the fetal telencephalon cell suspensions at the start of the culture period, successfully integrated into aggregate cultures. Supplementing the macrophage component of the cultures in this fashion resulted in increased accumulation of MBP. The effect of IFN‐γ on MBP content of cultures was not affected by the presence of macrophages in increased numbers. © 1994 Wiley‐Liss, Inc.
Human interleukin 1β: Corticotropin releasing factor and ACTH releasing and gene expression in the male rat: In vivo and in vitro studies
Authors: Parsadaniantz S. Mélik , Levin N. , Lenoir V. , Roberts J. L. , Kerdelhué B. 
Published: January 2005

AbstractNumerous studies have shown that interleukin 1 (IL1), a cytokine secreted by macrophages, is capable of stimulating the hypothalamo‐pituitary‐adrenai (HPA) axis. Nevertheless, the sites involved in IL1 stimulation of the HPA axis remain, to data, subjects of controversy. In the present study, using in vivo and in vitro approaches, we tried to characterize the route by which IL1 acts on the HPA axis. In vivo, after an i.p. injection of human IL1β (1μg/rat), we measured plasma ACTH concentration, anterior pituitary (AP) ACTH content, hypothalamic (HT) corticotropin releasing factor (CRF) content, and also AP pro‐opiomelanocortin (POMC) and HT CRF gene expression. ACTH and CRF were measured by specific radioimmunoassays (RIAs), and solution hybridization nuclease protection assay was used for quantification of nuclear POMC precursor RNA and nuclear and cytoplasmic POMC and CRF mRNA. Human IL1β provoked an increase in ACTH plasma concentration, a decrease in AP ACTH content, and a prolonged increase in AP POMC primary transcript levels (around 100%). A significant increase in APPOMC primary transcript content was evident 30 min after injection of hIL1β, while cytoplasmic POMC mRNA levels were increased in the AP only at 4 hr after injection of hIL1β. We did not observe an effect of hIL1β on either HT CRF content or HT CRF cytoplasmic mRNA levels. In order to characterize a possible direct effect of hIL1β; at the Ap level, we used an AP perifusion system to analyse the effect of hIL1β; and CRH on ACTH release and on POMC gene expression. CRF (10−9M) applied as a 10‐minpulse provoked a marked rise in ACTH release and an 80% increase (P < 0.05) in POMC primary nuclear RNA transcript. Treatment of AP with hIL1β; (10−9M or 10−10) for 60 min did not affect ACTH release or POMC primary nuclear RNA transcript levels. The present study would suggest that the acute effect of hIL1β on ACTH secretion and synthesis is probably not due to a direct action of hIL1β at the AP level, but could result from a direct or indirect effect of IL1β on the release and synthese of hypothalamic CRF. Wiley‐Liss, Inc.
Understanding the CD4 molecule: Surface expression and function
Authors: Morriso W. J. , Offner H. , Vandenbark A. A. 
Published: January 2005

AbstractSurface expression of the CD4 glycoprotein molecule is postulated to facilitate antigen recognition through the T cell receptor (TCR) and is itself a receptor for human immunodeficiency virus (HIV)‐gp120 glycoprotein. Both antigen‐stimulated TCR activation and HIV infectivity can be blocked by whole anti‐CD4 antibodies. Although selective modulation of CD4 from the surface by gangliosides (GM1) blocks HIV infectivity, it enhances associated TCR function. Enhanced TCR function has also been observed after intracellular delivery of synthetic CD4 mRNA‐antisense oligodeoxynucleotides (ODN) that block de novo synthesis of CD4. These specific CD4 modulations were mechanistically different from one another yet they both selectively removed the CD4 molecule from the T cell surface and enhanced antigen‐stimulated function through the TCR. The proposed role of CD4 during TCR function and HIV infectivity was developed, in part, according to decreases following CD4 antagonism by whole antibody or down‐modulation of CD4 by phorbol‐stimulated protein kinase C activity. Selective CD4 modulations have independently redefined the specific contributions of CD4 surface expression during T cell activation and may establish a role for CD4 receptor subtypes during HIV‐1 infenction of CD4+ cells. © 1994 Wiley‐Liss, Inc.
GO, a guanine nucleotide binding protein, is expressed during neurite extension in the embryonic mouse
Authors: Schmidt C. J. , Zubiaur M. , Valenzuela D. , Neer E. J. , Dräger U. C. 
Published: January 2005

AbstractThe developmental pattern of expression of the G protein αO subunit and GAP43 were compared by immunohistochemical staining of mouse embryos. Staining for αO and GAP43 was identical and detected throughout the developing nervous system, and the antigens first appeared in neurons at the beginning of neuronal differentiation. GAP43 and αO were not detected in regions containing only neuroblasts. These observations suggest that αO and GAP43 may not be required for the decision to pass from neuroblast to differentiated neuron, but may play a role in signal transduction during early neuronal development. © 1994 Wiley‐Liss, Inc.
Differentiation of oligodendrocytes cultured from developing rat brain is enhanced by exogenous GM3 ganglioside
Authors: Yim S. H. , Farrer R. G. , Hammer J. A. , Yavin E. , Quarles R. H. 
Published: January 2005

AbstractCultures consisting primarily of O‐2A progenitor cells and immature oligodendrocytes with a few microglia and astrocytes were obtained by shaking primary cultures from neonatal rat brain after 12‐‐14 days in vitro. Addition of 50 μg/ml exogenous Neu‐NAcα2‐3Galβ1‐1′ ceramide (GM3 ganglioside) to the cultures resulted in an increase in the number and thickness of cell processes that stained intensely for sulfatide and galactocerebroside (galC) in comparison to control cultures without added GM3. The treated cultures also contained fewer astrocytes than control cultures as revealed by immunostaining for glial fibrillary acidic protein (GFAP). Cells that immunostained for both GFAP and sulfatide/galC were very rare in control cultures but were frequently seen in the GM3‐treated cultures, suggesting that these may represent cells changing their direction of differentiation away from type II astrocytes toward oligodendrocytes under the influence of GM3. These effects on the developing rat oligodendrocytes were specific for GM3 ganglioside and were not produced by adding GM1, GM2, GD3, or GD1a to the cultures. Lactosyl ceramide and neuraminyl lactose were also ineffective. When control cultures were initially plated on polylysine and incubated with [14C]galactose, GD3 was the principal labeled ganglioside. However, as the control cells differentiated over time in culture without the addition of exogenous GM3 and produced increasing amounts of myelin‐related components, the incorporation of [14C]galactose into endogenous GM3 increased to become the predominant labeled ganglioside by 6 days after plating. Metabolic labeling of the GM3‐treated oligodendrocytes with [14C]galactose revealed increased incorporation into galC and sulfatide in comparison to control cultures, but a decreased labeling of endogenous GM3. Similarly, incorporation of an amino acid precursor into the myelin‐associated glycoprotein (MAG) was increased by GM3 treatment, but incorporation into myelin basic protein (MBP) was not affected. Although the overall effect of added GM3 was to decrease the phosphorylation of most proteins in the oligodendrocytes, including MBP, GM3 enhanced the phosphorylation of MAG. These findings indicate that GM3 ganglioside has an important role in the differentiation of cells of the O‐2A lineage toward myelin production, since differentiation is associated with increased metabolic labeling of endogenous GM3 in control cultures and is enhanced by the addition of exogenous GM3. © 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.
Serotonin inhibits outgrowth of goldfish retina and impairs the trophic effect of taurine
Authors: Lima L. , Matus P. , Urbina M. 
Published: January 2005

AbstractThe regeneration of explants prepared from goldfish retinas with a prior crush of the optic nerve is stimulated by the sulphur amino acid, taurine. Serotonin has been reported to modify survival, proliferation, and outgrowth of nervous tissue. In the present work we evaluated the effect of serotonin and some serotonergic agonists on the neuritic outgrowth from goldfish retinal explants. Serotonin, its precursor, 5‐hydroxytryptophan, and the 5HT1A receptor agonists, 8‐hydroxy‐2‐(di‐n‐propylamino)tetralin and busprione, inhibited the outgrowth. The blockers of serotonin uptake, imipramine and citalopram, were also inhibitors of neurite sprouting. Imipramine favoured the inhibitory effect of serotonin at 10 days in culture. The concentration of serotonin and its metabolite, 5‐hydroxyindoleacetic acid, decreased in the retina at 3 and 5 days after the crush of the optic nerve. Serotonin levels started to recover after 5 days post‐lesion, and the metabolite also increased. This indicates that the lesion increases the turnover rate of serotonin and this may be related to its role in regeneration. Serotonin concentration was elevated by the intraocular administration of its precursor, 5‐hydroxytryptophan, indicating that the capacity for synthesis was preserved after the crush, but that it was smaller in the post‐lesioned retinas. The trophic effect of taurine was impaired by a low concentration of serotonin, probably by opposing the final effect on growth via different targets. These results support a role of serotonin in the regeneration of goldfish retina probably through 5HT1A receptors. © 1994 Wiley‐Liss, Inc.
D2 dopamine receptor protein location: Golgi impregnation‐gold toned and ultrastructural analysis of the rat neostriatum
Authors: Fisher R. S. , Levine M. S. , Sibley D. R. , Ariano M. A. 
Published: January 2005

AbstractThe neostriatal distribution of D2 dopamine receptor protein has been assessed using subtype‐selective polyclonal antibodies generated against three unique polypeptide sequences of the receptor. The experimental tissues were processed by peroxidase based immunohistochemical procedures for routine light microscopy, Golgi impregnation‐gold toned morphological characterization, and correlative light/electron microscopy. The results demonstrated a regional gradient of D2‐like dopamine receptor expression in the neostriatum, where lateral portions in the nucleus exhibited more reactive cell bodies than medial portions. D2‐like expression was detected in the three populations of neostriatal neurons, i. e., the medium‐sized spiny projections neurons, and the medium‐ and large‐sized aspiny interneuron types. Morphometric measurements of labeled neurons verified that medium and large diameter neurons expressed the D2‐like receptor subtype. D2‐like immunoreactivity was distributed throughout the cytoplasm in dendritic processes, and in presynaptic terminal boutons. Immunoreactivity for the receptor protein was also detected in small, thinly myelinated axons, suggesting the possibilities of anterograde transport of the receptor from cell bodies in the substantia nigra to their neostriatal terminal fields, as well as from local axon collaterals of neostriatal projections neurons. These findings provide evidence of widespread distribution of the D2‐like receptor protein in neostriatal neurons, and showed that the presynaptic D2 receptors contain analogous epitopes to the postsynaptic receptor subtype. © 1994 Wiley‐Liss, Inc.
Expression of growth‐associated protein‐43 kD in Schwann cells is regulated by axon‐Schwann cell interactions and cAMP
Authors: Scherer S. S. , Xu Y.‐T. , Roling D. , Wrabetz L. , Feltri M. L. , Kamholz J. 
Published: January 2005

AbstractWe have examined the regulation of growth‐associated protein 43 kD (GAP‐43) in rat Schwann cells. In unlesioned adult nerves, GAP‐43‐immunoreactivity was restricted to non‐myelinating Schwann cells and unmyelinated axons. When adult nerves were transected to cause permanent axotomy, previously myelinating Schwann cells expressed progressively more GAP‐43‐immunoreactivity over 3 weeks and GAP‐43 mRNA levels increased over a similar time course. The peak level of GAP‐43 mRNA occurred at least 2 weeks later than that of nerve growth factor receptor, another marker of denervated Schwann cells. In contrast, after nerve‐crush, which allows axonal regeneration, many fewer Schwann cells had GAP‐43‐immunoreactivity, and the amount of GAP‐43 mRNA was markedly lower than in transected nerves. Forskolin, a drug that activates adenylate cyclase and mimics many effects of axon‐Schwann cell interactions, markedly reduced GAP‐43‐immunoreactivity and mRNA expression in cultured Schwann cells, whereas interleukin‐1 had no effect. These data demonstrate that axon‐Schwann cell interactions inhibit the expression of GAP‐43 in Schwann cells and that this effect is mimicked by forskolin. © 1994 Wiley‐Liss, Inc.
Decreased synaptic density in aged brains and its prevention by rearing under enriched environment as revealed by synaptophysin contents
Authors: Saito S. , Kobayashi S. , Ohashi Y. , Igarashi M. , Komiya Y. , Ando S. 
Published: January 2005

AbstractChanges in synaptic density in various brain regions were assessed among different age groups of rats maintained in ordinary small cages, as determined by synaptophysin assay. The synaptophysin content in hippocampus decreases as early as in the adult stage. The most remarkable decrement occurs in occipital cortex. In other regions, synaptophysin contents decrease in senescence to 60–77% of the respective peak values during young and adult stages. The other rat group reared under enriched environment in a large cage until 30 months of age was examined for synaptic density, and was revealed to maintain the similar levels as in young, or even higher levels in frontal, temporal, entorhinal cortices and hippocampus. These results indicate that the synaptic density in cerebrum decreases in senescence and this decrease can be prevented by rearing under enriched environment. © 1994 Wiley‐Liss, Inc.
G‐protein γ7 subunit is selectively expressed in medium‐sized neurons and dendrites of the rat neostriatum
Authors: Watson J. B. , Coulter P. M. , Margulies J. E. , de Lecea L. , Danielson P. E. , Erlander M. G. , Sutcliffe J. G. 
Published: January 2005

AbstractWe used subtractive hybridization to isolate clones of γ7, a 68 residue G‐protein γ subunit. Northern blotting and in situ hybridization reveal that the γ7 subunit mRNA is expressed primarily in medium‐sized neurons of the neostriatum and nucleus accumbens and neurons of the olfactory tubercle, and at low levels in the dentate gyrus of the hippocampal formation and laminae II–III, and V of the neocortex. The γ7 mRNA is translocated into dendrites of neurons in the neostriatum and the dentate gyrus of the hippocampus. γ7 is expressed at relatively very low concentrations in peripheral tissues. The selective pattern of γ7 expression within the brain is highly reminiscent of those of the striatum‐enriched adenylyl cyclase ACST, dopamine receptors, and the α subunit of Golf, suggesting that, in striatum, γ7 may be a subunit of a Golfα‐containing G protein that couples dopamine receptors selectively to ACST.Copyright © 1994 Wiley‐Liss, Inc.
Motoneuron survival is not affected by the proximo‐distal level of axotomy but by the possibility of regenerating axons to gain access to the distal nerve stump
Authors: Tõrnqvist E. , Aldskogius H. 
Published: January 2005

AbstractThe aim of this study was to examine whether axotomy‐induced motoneuron death in adult mammals differ: (1) with the distance between the site of injury and the nerve cell body, and (2) if contact between the transected nerve stumps is established after the injury, compared with cases where contact is prevented.The hypoglossal nerve of adult rats was transected either proximally in the neck (proximal injury) or close to the tongue (distal injury). The nerve stumps were then either deflected from each other in order to prevent axon regeneration into the distal nerve stump, or sutured. Three months later, the extent of nerve cell loss was examined bilaterally in cresyl violet‐stained sections of the hypoglossal nucleus. In addition, we examined hypoglossal neuron survival twelve months after a proximal nerve transection with prevented regeneration.Our results show that there was no significant difference in neuronal survival after a proximal nerve transection compared with a distal one, neither if contact between the nerve stumps was established nor if it was prevented. However, contact between the transected nerve stumps increased the likelihood of neuronal survival significantly after both proximally and distally located injury compared to nerve injury with prevented regeneration. There was no significant decrease in nerve cell survival after twelve months with prevented reinnervation compared with survival after three months.These observations indicate that the extent of axotomy‐induced motoneuron death in adult mammals does not correlate with the proximo‐distal level of peripheral injury. Furthermore, early contact with the distal stump and/or target musculature is a significant factor for the survival of axotomized motoneurns. However, more than 50% of the original nerve cell population survives a considerable time even after permanent disconnection from the target. Copyright © 1994 Wiley‐Liss, Inc.
Effects of the N‐acetylgalactosaminyltransferase inhibitor on cultured cerebral cells
Authors: Grabois V. R. , Conde C. B. , Caputto R. 
Published: January 2005

AbstractThe inhibitor preparation of the UDP‐N‐acetylgalactosamine: GM3, N‐acetylgalactosaminyltransferase (EC 2.4.1.92) (GalNAc‐T) produces effects on the neurons and the glial (astrocytes) cells of the cerebrum in culture. The effect in culture is evidenced by aneuritogenesis, deficiency in the GalNAc‐T activity, and decrease in the content of gangliosides, proteins, and lipids. In isolated glial cells the effect is evidenced by cytoplasm vesiculation and premature cessation of proliferation compared with control culture. The pattern of gangliosides in the inhibited culture shows a decrease in the amount of GD1a with respect to GD3; this is compatible with the notion that the effect is due to an inhibitor of the GM2 synthase. The inhibitor effects are reverted when it is eliminated after 24 or 48 hr in the culture medium. © 1994 Wiley‐Liss, Inc.
Enhanced aggregation and β structure of amyloid β peptide after coincubation with C1Q
Authors: Webster S. , O'Barr S. , Rogers J. 
Published: January 2005

AbstractSeveral lines of evidence now suggest that aggregation of soluble amyloid β peptide (Aβ) into a cross β sheet configuration may be an important factor in mediating potential neurotoxicity of Aβ. Synthetic Aβ has been shown to self aggregate in vitro. Here, we demonstrate that coincubation of freshly solubilized Aβ with C1q, a complement component known to bind Aβ in vitro and to colocalize with Aβ in vivo, results in as much as a 7‐fold enhancement of Aβ aggregation, as well as a 2–4‐fold enhancement of β structure within aggregates. The addition of C1q to preformed Aβ aggregates also results in significantly increased resistance to aggregate resolubilization. © 1994 Wiley‐Liss, Inc.
Inhibitors of free radical formation fail to attenuate direct β‐amyloid25–35 peptide‐mediated neurotoxicity in rat hippocampal cultures
Authors: Lockhart B. P. , Benicourt C. , Junien J.‐L. , Privat A. 
Published: January 2005

AbstractThe direct neurotoxic action of the β‐amyloid protein, the major constituent of senile plaques, may represent the underlying cause of neuronal degeneration observed in Alzheimer's disease. The apoptotic‐mediated neuronal death induced by β‐amyloid appears to reside in its ability to form Ca>2+‐permeable pores in neuronal membranes resulting in an excessive influx of Ca2+ and the induction of neurotoxic cascades. It is possible that during β‐amyloid exposure a Ca2+‐mediated increase in free radical generation may exceed the defensive capacity of cells and thus lead to cell death. Consequently, in the present study we have investigated the effect of a panoply of antioxidants and inhibitors of free radical formation on the development of β‐amyloid neurotoxicity. Acute exposure of rat hippocampal neurons to “aged” β‐amyloid25–35 peptide (5–50 m̈M) induced a slow, concentration‐dependent apoptotic neurotoxicity (25–85%) during a 6 day exposure. Co‐incubation of cultures with β‐amyloid25–35 peptide (25 μM) and inhibitors of nitric oxide synthase and/or xanthine oxidase (NG‐monomethyl‐L‐arginine [1 mM], Nω‐nitro‐L‐arginine [1 mM], oxypurinol [100 m̈M], allopurinol [100 m̈M]), important mediators of nitric oxide, superoxide, and hydroxyl radical formation, did not attenuate β‐amyloid neurotoxicity. Similarly, a reduction in free radical generation by selective inhibition of phospholipase‐A2 cyclooxygenase, and lipoxygenase activities with quinacrine (0.5 m̈M), indomethacin (50 m̈M), and nor‐dihydroguaiaretic acid (0.5 m̈M), respectively, did not reduce the proclivity of β‐amyloid to induce cell death. Exposure of cultures to catalase (25 U/ml) and/or superoxide dismutase (10 U/ml) as well as the free radical scavengers vitamin E (100 m̈M), vitamin C (100 m̈M), glutathione (100 m̈M), L‐cysteine (100 m̈M), N‐acetyl‐cysteine (100 m̈M), deferoxamine (5 m̈M), or haemoglobin (35 m̈g/ml) failed to attenuate the neurotoxic action of β‐amyloid. On the other hand, pre‐treatment of cultures with subtoxic concentrations of β‐amyloid peptide significantly increased the vulnerability of neurons to H2O2 exposure and suggest that β‐amyloid peptide renders neurons more sensitive to free radical attack. However, a potential β‐amyloid‐mediated increase in free radical formation is not a proximate cause of the neurotoxic mechanism of β‐amyloid in vitro. © 1994 Wiley‐Liss, Inc.