bluuebunny/crossref_metadata_2025_split huggingface dataset:
The differentiation and survival of murine neurons in vitro is promoted by soluble factors produced by an astrocytic cell line
Authors: Kilpatrick T. J. , Talman P. S. , Bartlett P. F. 
Published: January 2005

AbstractThe influence of accessory cells on the generation of neurons and neuronal survival has been studied in vitro using an immortalised, cloned cell line, Ast‐1, which has many of the functional and phenotypic characteristics of cells of the astrocytic lineage. It was found that monolayers of Ast‐1 cells were equivalent to monolayers of primary astrocytes in their ability to promote the generation of neurofilament positive neurons from neuroepithelial cells obtained from embryonic day 10 (E10) mice; and both were superior to NIH 3T3 cells. Ast‐1 cell monolayers were also found to provide a suitable substrate for the prolonged survival (at least 3 days in vitro) of neurofilament positive neurons obtained from E17 mice, whereas neurons plated onto NIH 3T3 cells were all dead after 2 days. Medium conditioned by Ast‐1 cells displayed similar biological activities to that of the monolayers: It increased the number of neurons generated from the E10 neuroepithelial cells, whether they were plated directly onto glass coverslips or onto monolayers of NIH 3T3 cells; and it increased the survival of E17 neurons plated directly onto glass coverslips. In addition, the Ast‐1 conditioned medium was shown to promote the survival of the neuroepithelial cells. These results confirm that one of the mechanisms by which astrocytes or their precursors may regulate neuronal development is by secreting soluble growth factors, as has been previously documented in the case of fibroblast growth factor (FGF) (Hatten et al., 1988; Drago et al., 1991a). However, it appears in this system that FGF is not responsible for the demonstrated biological activities, and the Ast‐1 action appears to be mediated by putatively novel factor(s). © 1993 Wiley‐Liss, Inc.
Nitric oxide induces calcium‐dependent release of [3H]dopamine release from striatal slices
Authors: Lonart G. , Cassels K. L. , Johnson K. M. 
Published: January 2005

AbstractHydroxylamine (0.01–30 mM), a nitric oxide (NO) generator, produced a concentration‐dependent release of [3H]dopamine ([3H]DA) from rat striatal slices. Hemoglobin (10 μM), a NO scavenger, reduced basal [3H]DA release and blocked hydroxylamine (100 μM)‐stimulated [3H]DA efflux. Tetrodotoxin (0.5 μM) had no significant effect. Sodium cyanide was used as a model compound to test the possibility that NO acted through blockade of mitochondrial electron transport. Calcium‐free experimental buffer (1 mM EGTA) reduced basal release and the hydroxylamine response, while sodium cyanide‐induced release did not change under these experimental conditions. Cadmium (200 μM), a non‐selective inhibitor of voltage‐dependent calcium channels, reduced the hydroxylamine response by 69%. Methylene blue (10 μM), an inhibitor of guanylate cyclase, produced a 3‐fold increase in the basal release but had no significant effect on the hydroxylamine response. These data suggest that NO induces calcium‐dependent [3H]DA release from the striatum via a mechanism which is independent of blockade of electron transport or activation of guanylate cyclase. © 1993 Wiley‐Liss, Inc.
Axon growth is enhanced by NCAM lacking the VASE exon when expressed in either the growth substrate or the growing axon
Authors: Liu L. , Haines S. , Shew R. , Akeson R. A. 
Published: January 2005

AbstractThe neural cell adhesion molecule NCAM exists as several related peptides formed by alternative splicing of the single NCAM gene. Here the ability of NCAM containing and lacking the alternatively spliced VASE exon to act as a permissive growth substrate was tested by examining retinal axon outgrowth on normal L cell fibroblasts and L cells expressing stably transfected 140 kD NCAM ± VASE. L cells expressing either NCAM form were a more permissive substrate than control L cells. At higher substrate cell densities, greater axon outgrowth occurred on substrate cells expressing NCAM − VASE than on those expressing NCAM + VASE. Similar experiments tested retinal axon growth on neuronal substrates by utilizing clonal B35 cells, C3 cells that are NCAM lacking variants of B35, and C3 cells into which 140 kD NCAM ± VASE has been restored by transfection. Axon growth on C3 cells transfected with NCAM − VASE was greater than that on all other substrates including cells transfected with NCAM + VASE. In these experiments C3 cells and transfected C3 expressing NCAM + VASE cell promoted similar outgrowth. The influence on neurite growth of the NCAM isoform of the neurite itself was tested by examining neurite formation using combinations of C3 cells and C3 NCAM transfectants both in the growth monolayer and as responding cells. C3 cells were able to extend neurites, indicating NCAM is not required for neurite growth. However, C3 derivatives transfected with NCAM ± VASE had greater neurite outgrowth. The most extensive neurite growth was found when NCAM − VASE was expressed by both substrate cells and the responding neurite growing cells. Thus NCAM enhances axon or neurite outgrowth when present either in the growth substrate or on the growing axon. NCAM − VASE has a significantly greater growth promoting capability than NCAM + VASE. The expression of NCAM + VASE by more mature neural cells could thus be a © Wiley‐Liss, Inc. significant factor in the reduced axonation capabilities of mature neurons. © 1993 Wiley‐Liss, Inc.
Retinoic acid induces cholinergic differentiation of cultured newborn rat sympathetic neurons
Authors: Berrard S. , Biguet N. Faucon , Houhou L. , Lamouroux A. , Mallet J. 
Published: January 2005

AbstractMany studies provide evidence that retinoic acid (RA), an endogenous derivative of vitamin A, plays a role in the development of the nervous system. We now report that RA controls the neurotransmitter phenotype of post‐mitotic rat sympathetic neurons in cell culture. RA added to the culture medium increased the specific activity of choline acetyltransferase (ChAT) and the level of acetylcholine (ACh). Concomitantly, RA reduced the specific activities of two catecholamine synthetic enzymes, tyrosine hydroxylase (TH) and dopamine β‐hydroxylase (DBH) and the level of norepinephrine (NE). After a 2 week treatment with 5 μM RA, ChAT was increased by 5–10 fold, whereas TH and DBH were decreased by 10–15 fold and 2–3 fold, respectively, as compared to sympathetic neurons grown in the absence of RA. The modulation of the activity of the three enzymes was dose‐dependent and followed a similar time course. The decrease of TH expression was demonstrated to be due to a decreased number of TH molecules. © 1993 Wiley‐Liss, Inc.
Vesicular transport of myelin proteolipid and cerebroside sulfates to the myelin membrane
Authors: Brown M. C. , Moreno M. Besio , Bongarzone E. R. , Cohen P. D. , Soto E. F. , Pasquini J. M. 
Published: January 2005

AbstractThe possibility that cerebroside sulfates and myelin proteolipid (PLP) could be simultaneously located in transport vesicles destined to be assembled in myelin was investigated in the brain of 20 day old rats. The brain was homogenized and fractionated according to Burkart et al. (J Biol Chem 257:3151–3156, 1982) to obtain a microsomal fraction that was further subfractionated in a linear sucrose density gradient following the procedure of Siegrist et al. (J Neurochem 33:497–504, 1979) to obtain a vesicular fraction which has been shown to transport cerebroside sulfates (Burkart et al., as above). This fraction was associated with acid hydrolase activity and had a lipid composition different from that of myelin and microsomal fractions. Studied by slab gel electrophoresis, dot blot, and Western blot analysis, using a highly specific anti‐PLP antibody, it was found to contain myelin PLP. In view of previous findings of several laboratories including our own, the presence of myelin proteolipid in a vesicular fraction which is related to the transport of cerebroside sulfates gives further support to the hypothesis that the delivery of both constituents to the myelin membrane could be associated. © 1993 Wiley‐Liss, Inc.
Changes of amino acid and monoamine levels after neonatal 6‐hydroxydopamine denervation in rat basal ganglia, substantia nigra, and raphe nuclei
Authors: Molina‐Holgado E. , Dewar K. M. , Grondin L , van Gelder N. M. , Reader T. A. 
Published: January 2005

AbstractThe effects of a neonatal dopaminergic deafferentation with the neurotoxin 6‐hydroxydopamine (6‐OHDA) on endogenous tissue levels of catecholamines, indoleamines, and amino acids were investigated in discrete rat brain regions. After producing the lesion at postnatal day 3 by intraventricular injections of 6‐OHDA, with a desipramine pretreatment to protect noradrenaline neurons, the animals were kept for 3 months. Their brains were dissected to obtain samples of neostriatum, Globus pallidus, Substantia nigra, and Raphe nuclei, which were then analyzed by high‐performance liquid chromatography, coupled either to electrochemical detection for aromatic monoamines, or to post‐column ninhydrin derivatization with spectrophotometry for amino acids. The neonatal 6‐OHDA treatment depleted dopamine (DA) levels in neostriatum, Globus pallidus, and Substantia nigra, but in Raphe nuclei DA was increased. The main metabolites of DA were also decreased in neostriatum, Globus pallidus, and Substantia nigra but remained unchanged in Raphe nuclei. Serotonin (5‐HT) and its metabolite 5‐hydroxyindole‐3‐acetic acid increased in neostriatum and Raphe nuclei; in Substantia nigra there was a slight increase in 5‐HT only. The 6‐OHDA lesion caused heterogeneous alterations in amino acid contents, which varied according to the region. In the neostriatum there were increases of γ‐aminobutyric acid (GABA), aspartic acid, and glycine. In the Globus pallidus taurine, GABA, glutamic acid, glutamine, aspartic acid, serine, and alanine were elevated. In the Substantia nigra only increases in taurine, GABA, glutamic acid, and glutamine could be documented. This study shows important changes in amino acid levels and in some of their ratios, occurring in different anatomical subdivisions of the basal ganglia and related brainstem nuclei following a neonatal treatment with 6‐OHDA. The results thus demonstrate major biochemical modifications in amino acids in the aftermath of a DA denervation and/or a 5‐HT hyperinnervation during an early developmental period. © 1993 Wiley‐Liss, Inc.
mRNAs Coding for neurotransmitter receptors in rabbit and rat visual areas
Authors: Matute C. , Nguyen Q.‐T. , Miledi R. 
Published: January 2005

AbstractLevels of mRNAs encoding neurotransmitter receptors in the visual cortex, lateral geniculate nucleus, and superior colliculus of the rabbit and rat, and properties of the receptors expressed, were studied using Xenopus laevis oocytes. mRNA extracted from these areas was injected into the oocytes, which then acquired functional receptors. Electrical recordings of neurotransmitter‐induced membrane currents reflect the relative amounts of mRNAs encoding the corresponding receptors. Receptors to gamma aminobutyric acid (GABA), kainate, glutamate, and serotonin exhibited uniformly high levels of expression, whereas expression of receptors to glycine and N‐methyl‐D‐aspartate was uniformly low. In contrast, the expression of receptors to acetylcholine and substance P was highly non‐uniform. Expression of acetylcholine receptors was high in oocytes injected with mRNA from the visual cortex, low for the lateral geniculate nucleus, and very low or absent for the superior colliculus. Conversely, the currents elicited by substance P were large in oocytes injected with superior colliculus mRNA, but were small or absent in oocytes injected with mRNAs from the other regions. Immunohistochemical analysis, at the light and electron microscopic levels, was used to localize choline acetyltransferase, the acetylcholine‐synthesizing enzyme, and substance P‐containing synaptic boutons in the three visual areas. Their presence closely paralleled the potency of mRNAs coding for acetylcholine and substance P receptors. The ability of rat mRNA, from each visual area, to induce neurotransmitter receptors was similar to that observed in the corresponding rabbit mRNAs. In addition to the marked differential distribution of mRNA encoding neurotransmitter receptors in the visual system, our findings reveal the probable existence of as yet uncharacterized receptors, whose new molecular forms may be revealed by further study. Our results also provide the basic information required for subsequent studies on the effect of monocular deprivation on the expression of neurotransmitter receptors in the visual system. © 1993 Wiley‐Liss, Inc.
Nerve growth factor and p75NGFR factor receptor mRNA change in rodent CNS following stress activation of the hypothalamo‐pituitary‐adrenocortical axis
Authors: Foreman P. J. , Taglialatela G. , Angelucci L. , Turner C. P. , Perez‐Polo J. R. 
Published: January 2005

AbstractThe synthesis of nerve growth factor (NGF) by the hippocampus raises the possibility that NGF may play a role in the regulation of the hypothalamic‐pituitary‐adrenal axis (HPAA). Subchronic cold stress has been shown to activate the HPAA in a mild noninvasive manner, to stimulate serum glucocorticoid levels, and to perturb NGF binding in hippocampus and basal forebrain. One or repeated episodes of cold stress increased NGF mRNA levels in the hippocampus and p75NGFR mRNA levels in the basal forebrain. These changes were not due to elevated serum glucocorticoid levels since treatment with exogenous corticosterone had no effect on NGF and p75NGFR mRNA levels. Adrenalectomy did not prevent the stress induced increases in NGF and p75NGFR mRNA. © 1993 Wiley‐Liss, Inc.
Possible role of myelin‐associated neuraminidase in membrane adhesion
Authors: Saito M. , Yu R. K. 
Published: January 2005

AbstractPrevious studies from our laboratory have demonstrated the presence of a specific interaction between myelin‐associated neuraminidase and GM1 (Saito and Yu, J. Neurochem 47:632–641, 1986). In the present study, we further characterized this neuraminidase‐GM1 interaction and examined its role in the adhesion of rat oligodendroglial cells to GM1. Hydrolysis of N‐acetylneuramin‐lactitol by the enzyme was inhibited by GM1 in a competitive manner; GM1 itself was not hydrolyzed, suggesting that GM1 may serve as a competitive inhibitor of the enzyme. Asialo‐GM1 had no inhibitory effect. When a soluble enzyme preparation was applied to a GM1‐linked affinity column, the enzyme activity was retained on the column and was recovered from the column only by elution with a buffer containing 5 mM 2,3‐dehydro‐2‐deoxy‐N‐acetylneuraminic acid (Neu2en5Ac), a competitive inhibitor of neuraminidase. A binding study with 51 Cr‐labeled rat oligodendroglial cells showed that oligodendroglial cells bound preferentially to GM1 developed on a thin‐layer plate, but not to other gangliosides such as GM3, GD1a, GD1b, and GT1b. The binding reaction to GM1 was inhibited by Neu2en5Ac (5 mM). These results suggest that myelin‐associated neuraminidase specifically interacts with GM1 and may be involved in adhesion of oligodendroglial cells to GM1. This neuraminidase‐GM1 interaction may play an important role in the formation and stabilization of the multilamellar structure of the myelin sheath. © 1993 Wiley‐Liss, Inc.
Effect of hyaluronidase on brain extracellular matrix in vivo and optic nerve regeneration
Authors: Tona A. , Bignami A. 
Published: January 2005

AbstractIn the rat, intracerebral injection of bacterial hyaluronidase resulted in the almost complete disappearance of hyaluronic acid (HA) and glial hyaluronate‐binding protein (GHAP) from cerebral hemispheres, brain stem, and cerebellum (but not from optic nerves and chiasm) starting 2–3 hr after the injection. HA and GHAP reappeared throughout the brain in characteristic patches 2–3 days after the injection. The patches gradually became confluent and after 12 days the brain appeared virtually normal. In normal rat optic nerve, staining for HA and GHAP ceased abruptly in the region of the lamina cribrosa. The retina was completely negative. HA and GHAP disappeared from hyaluronidase‐injected optic nerve, chiasm, and contralateral optic nerve. In hyaluronidase‐injected crushed optic nerves, regenerated axons were able to grow for short distances (about 500μm) into the distal stump undergoing Wallerian degeneration. No such growth was observed in saline‐injected controls. © 1993 Wiley‐Liss, Inc.
Calcitonin induces a decreased Na+ conductance in identified neurons of Aplysia
Authors: Sawada M. , Ichinose M. , Ishikawa S. , Sasayama Y. 
Published: January 2005

AbstractThe ionic mechanism of the effect of extracellularly ejected calcitonin (CT) on the membrane of identified neurons R9 and R10 of Aplysia was investigated with voltage‐clamp, micropressure ejection, and ion substitution techniques. Micropressure‐ejected CT caused a marked hyperpolarization in the unclamped neuron. Heat‐inactivated CT was without effect. Clamping the same neuron at its resting potential level (−60mV) and re‐ejecting CT with the same dose produced a slow outward current (Io(CT), 30–40 sec in duration, 4–6 nA in amplitude) associated with a decrease in input membrane conductance. Io (CT) was decreased by depolarization and increased by hyperpolarization. The extrapolated reversal potential of Io was approximately +10mV. Io (CT) was sensitive to changes in the external Na+ concentration but not to changes in K+, Ca2+, and CI− concentrations. Micropressure‐ejected forskolin produced a slow outward current, which, like the current to CT, was associated with a decrease in input membrane conductance, and was sensitive to changes in the external Na+ concentration. Io (CT) was prolonged by bath‐applied isobutylmethylxanthine (IBMX) but was not affected by I‐oleoyl‐2‐acetylglycerol (OAG) and calphostin C. Neither superfusion of the neuron with nordihydroguaiaretic acid (NDGA) nor superfusion with indomethacin caused any changes in Io(CT). These results suggest that extracellular CT can induce a slow outward current associated with a decrease in Na+ conductance, mediated by a receptor‐controlled increase in intracellular cyclic adenosine 3′, 5′‐monophosphate. © 1993 Wiley‐Liss, Inc.
Cell type‐ and differentiation‐dependent expression from the mouse acetylcholine receptor ϵ‐subunit promoter
Authors: Sunyer T. , Merlie J. P. 
Published: January 2005

AbstractThe nicotinic acetylcholine receptor (AChR) in adult skeletal muscle is composed of α‐, β‐, ϵ‐, and δ‐sub‐units and is localized at the neuromuscular junction; in contrast, the more diffusely distributed fetal form is composed of α‐, β‐, γ‐, and δ‐subunits. To define sequences necessary for the transcriptional regulation of the mouse ϵ‐subunit gene, we sequenced and analyzed 1036 bp upstream of the transcription start site. Using deletion analysis of the 5′‐flanking region linked to the bacterial chloramphenicol acetyltransferase (CAT) gene and transfection of the resulting constructs into established cell lines, we demonstrate that a 151 bp fragment exhibits cell type‐ and differentiation‐specific promoter activity. This activity was independent of a myogenic factor putative binding site (E‐box). However, transactivation experiments with recombinant myoD, myogenin, or MRF4 showed that the E‐box was functional and that MRF4 preferentially transactivates the ϵ‐promoter. Thus, like other AChR promoters, the proximal region of the ϵ‐promoter contains information for cell type‐specific and developmental regulation of CAT and can be transactivated by myogenci factors in cultured cell lines. Unlike the other AChR promoters characterized to date, ϵ‐promoter function can be partially independent of myogenic factors of the helix‐loop‐helix class. © 1993 Wiley‐Liss, Inc.
Induction of c‐fos by excitatory amino acids in developing chick retina is affected by changes in cellular interactions
Authors: Pearlman E. M. , Seigel G. M. , Notter M. F. D. 
Published: January 2005

AbstractCell contact is important for normal maturation of chicken retinal Muller cells. In order to gain a better understanding as to how this occurs, we examined the ability of retinal cells with altered cell contacts to respond to an environmental stimulus. The response of Muller cells cultured under conditions which alter cell contacts was measured by activating intracellular signaling systems leading to induction of the earlyinducible gene c‐fos. Chicken retinal cells were cultured as explants, reaggregates, and monolayers and exposed to extracellular stimuli in the form of the excitatory amino acids D, L‐alpha aminoadipic acid (AAA) and N‐methyl‐D, L‐aspartic acid (NMDA). Each culture was exposed to 1.25 mM AAA, 2.5 mM AAA,50 μM NMDA, or 100 μM NMDA. Toxicity was assessed histologically and by immunocytochemical labeling of Müller cells after 2 days of exposure. Activation of c‐fos was determined by Western blot analysis for Fos protein after 30,60, and 120 minutes of exposure. Exposure to AAA led to a loss of Muller cells in explant and reaggregate cultures; however, Muller cells in monolayer culture; however, Muller cells in monolayer culture were not susceptible to AAA at either dose. NMDA was toxic to a specific population of neurons under all three culture conditions. Fos protein expression paralleled the histologic findings. Fos protein was significantly elevated after exposure to either dose of AAA in explant and reaggregate cultures but not in monolayer cultures. Monolayer and reaggregate cultures did not exhibit a significant increase in Fos levels in response to either dose of NMDA. Explant cultures exhibited an equivical response to only the 50 μM NMDA. These results suggest that the ability of Müller cells to respond to AAA by increasing levels of Fos protein requires that specific cell contacts occur during development. © 1993 Wiley‐Liss, Inc.
Myelin‐associated glycoprotein is phosphorylated by protein kinase C
Authors: Kirchhoff F. , Hofer H.‐W. , Schachner M. 
Published: January 2005

AbstractThe myelin‐associated glycoprotein (MAG) is a neural recognition molecule involved in heterophilic interactions between myelin‐forming cells and neurons. To characterize the molecular mechanisms underlying post‐translational modifications which may be instrumental in signal transduction following the recognition event, we have studied the stimuli leading to modification of 32P‐orthophosphate incorporation into MAG in cultures of oligodendrocytes or transformed differentiated Schwann cells. Here we show that in oligodendrocytes both the 67 and 72 kD isoforms of MAG were phosphorylated exclusively on serine, while in the transformed Schwann cells only the 67 kD isoform was found to be present and phosphorylated. The phorbol‐12‐myristoyl‐13‐acetate (PMA) did not affect biosynthesis of the protein backbone, but enhanced incorporation of phosphate by a factor of 2–3, indicating the involvement of protein kinase C. Exclusive phosphorylation of serine residues was also observed, when purified MAG was incubated with protein kinase C in the presence of [γ‐32P] ATP. In searching for the physiological stimuli which may trigger phosphorylation of MAG, cultures of oligodendrocytes were exposed to extracellular signals, such as coculture with dorsal root ganglion and spinal cord neurons carrying the MAG receptor, to membrane fractions of these neurons, monoclonal MAG antibody 513 binding to the recognition site of MAG, or platelet‐derived growth factor. None of these additives modified the phosphorylation of MAG. These observations point to the possibility that phosphorylation of MAG is controlled by yet unknown intracellular cues rather than by extracellular signals interacting with cell surface receptors of oligodendrocytes. © 1993 Wiley‐Liss, Inc.