bluuebunny/crossref_metadata_2025_split huggingface dataset:
Retinoic acid regulates the development of oligodendrocyte precursor cells in vitro
Authors: Laeng P. , Décimo D. , Pettmann B. , Janet T. , Labourdette G. 
Published: January 2005

AbstractCultures of oligodendrocyte precursor cells can be grown from brain hemispheres of newborn rats. These cells, also called O‐2A progenitor cells, can differentiate in vitro into oligodendrocytes or type 2 astrocytes. Basic FGF and PDGF are known to stimulate their proliferation and delay their differentiation. Lack or excess of retinoic acid (RA) has been known for a long time to alter brain development suggesting that this compound is involved in normal brain development. Here we report that RA partially inhibits both the proliferation and the differentiation of oligodendrocyte precursor cells. It also down‐regulates the mitogenic effect of bFGF on these cells while keeping them in an immature stage. RA is more effective than bFGF in inhibiting myelin basic protein mRNA expression in these cells, and like bFGF, it preserves their bipotential character. RA nuclear receptors RAR‐α and their transcripts are expressed in oligodendrocyte precursor cells as seen by Western blot, Northern blot and in situ hybridization. The expression of RAR‐α transcripts is stimulated transiently by RA alone or associated to bFGF. The expression of RAR‐β transcripts is not constitutive and is induced by RA alone or associated to bFGF and to a lesser extent by bFGF alone. These results suggest that retinoids participate in the control of the development of glial cells of the oligodendrocyte lineage. © 1994 Wiley‐Liss, Inc.
Supraspinal delta opioid receptor mRNA levels are not altered in [D‐Ala2]Deltorphin II tolerant mice
Authors: Kest B. , Jenab S. , Brodsky M. , Elliott K. , Inturrisi C. E. 
Published: January 2005

AbstractDelta opioid receptor (DOR) mRNA levels were studied in mice rendered tolerant to [D‐Ala2]deltorphin II by 4 days of repeated intracerebroventricular administration (10μg, [tid]). ED50 determinations on day 5 revealed a 10‐fold loss in [D‐Ala2]deltorphin II potency with the tail‐flick test. Utilization of a microdissection technique followed by quantitative solution hybridization of RNA extracts from mouse brain revealed mean levels of DOR mRNA ranging from 3.9 pg/μg RNA in the caudate‐putamen to 0.4 pg/μg RNA in the cerebellum. DOR mRNA levels were not different when RNA extracts from tolerant and nontolerant mice were compared. These data suggest that altered DOR mRNA levels are not one of the adaptive changes that occur with delta opioid ([D‐Ala2]deltorphin II) tolerance. © 1994 Wiley‐Liss, Inc.
Age‐related increases in glial fibrillary acidic protein do not show proportionate changes in transcription rates or DNA methylation in the cerebral cortex and hippocampus of male rats
Authors: Laping N. J. , Teter B. , Anderson C. P. , Osterburg H. H. , O'Callaghan J. P. , Johnson S. A. , Finch C. E. 
Published: January 2005

AbstractAge‐related increases in the expression of glial fibrillary acidic protein (GFAP) in many brain regions are observed in short‐ and long‐lived mammals. Possible genomic mechanisms for the increase of GFAP mRNA and protein were studied in the hippocampus and cortex of male F344 rats and a longer‐lived hybrid F1(F344 × Brown Norway). No age‐related changes were found in the extent of cytosine methylation at 19 CpG sites in the 5′‐upstream GFAP promoter and in exon 1. With the nuclear runon assay, no change was found in the transcription rate of GFAP in the cerebral cortex or hippocampus. Thus, age‐related increases in GFAP are not associated with proportionate changes in transcription rates or DNA methylation. However, the transcription of glutamine synthetase was increased by about 60%. These findings contrast with age‐related loss of bulk tissue DNA methylation and decreased transcription rates of other genes reported in non‐neural tissues. © 1994 Wiley‐Liss, Inc.
NGF protects PC12 cells against ischemia by a mechanism that requires the N‐kinase
Authors: Boniece I. R. , Wagner John A. 
Published: January 2005

AbstractNerve growth factor (NGF), which has been shown to act as a morphological and neurochemical differentiating factor in PC12 cells, also protects PC12 cells from the toxicity of serum withdrawal and ischemia. By using a previously established in vitro model of ischemia, which incorporates the combination of anoxia with glucose deprivation (Boniece and Wagner: J Neurosci 13:4220–4228, 1993), we have been able to study the signal transduction pathways upon which NGF‐induced survival is dependent. Here we demonstrate that inhibitors of the N‐kinase and NGF‐induced neuritogenesis, 6‐thioguanine and 2‐aminopurine, prevent the protective effects of NGF, while they have little, if any, effect on the protection conferred by epidermal growth factor (EGF) or dbcAMP. This suggests that only NGF acts by a mechanism that depends strongly on the N‐kinase. Furthermore, the methyltransferase inhibitor 5′‐deoxy‐5′‐methylthioadenosine (MTA), which also inhibits NGF‐induced neuritogenesis, inhibits the protective effect of NGF but not the protective effects of EGF or dbcAMP. Thus, the neuroprotective effect of NGF requires some of the same signal transduction steps used by NGF to promote differentiation and neurite formation. Furthermore, we found that exposure of PC12 cells to retinoic acid, which promotes the differentiation and inhibits the growth of PC12 cells, also improves cell survival during ischemia. In addition, a combination of NGF and retinoic acid was more effective than either agent alone. It is likely that these two agents confer protection by independent pathways. © 1995 Wiley‐Liss, Inc.
Hypoosmotic volume regulation of astrocytes in elevated extracellular potassium
Authors: Olson James E. , Alexander C. , Feller D. A. , Clayman M. L. , Ramnath E. M. 
Published: January 2005

AbstractCellular volume and potassium contents were determined in rat astrocytes from primary culture following suspension in isoosmotic (269 mOsm) and hypoosmotic (136 mOsm) phosphate‐buffered saline (PBS) containing various potassium concentrations. Within 1 min of suspension in hypoosmotic PBS, cells swelled to 135% of their volume in isoosmotic PBS. This initial swelling was not altered by varying the potassium concentration of the hypoosmotic PBS. After suspension in hypoosmotic PBS containing 3.2 mM potassium, a regulatory volume decrease (RVD) was observed. Higher concentrations of potassium in hypoosmotic PBS inhibited RVD following osmotic swelling. Cells swollen in hypoosmotic PBS containing 50 mM potassium continued to swell for 7 min, reaching a volume of 141 % of their initial isoosmotic volume. After 7 min, these cells demonstrated a subsequent decrease in volume. The swelling observed between 1–7 min after suspension in hypoosmotic PBS containing 50 mM potassium was not affected by 10 μM gadolinium, 1 mM quinine, 1mM DIDS (4,4′‐diisothiocyanato‐2,2′‐stilbenedisulfonic acid), 1 mM SITS (4‐acetamido‐4′‐isothiocyanato‐2,2′‐stilbenedisulfonic acid), 1 mM furosemide, or 100 μM bumetanide. Normal RVD was obtained in hypoosmotic PBS containing 50 mM potassium, if chloride was replaced with gluconate (but not nitrate) to reduce the extracellular K‐C1 product to that of hypoosmotic PBS containing 3.2 mM potassium. The volume decrease seen between 7–30 min after exposure to hypoosmotic PBS containing 50 mM potassium was blocked by 1 mM DIDS, 1 mM SITS, or 1 mM furosemide. Cellular potassium content was elevated by approximately 60% after 7 min exposure to isoosmotic or hypoosmotic PBS containing 50 mM potassium. In hypoosmotic PBS, this increase in cellular potassium was reduced with replacement of chloride by gluconate, but not by nitrate. The results indicate that astrocytes swollen in PBS containing elevated potassium concentrations continue to swell, in part, by accumulation of potassium plus chloride mediated by an approach to Donnan equilibrium. Cotransport carriers or stretch‐activated channels do not play a role in the enhanced swelling observed in hypoosmotic PBS containing 50 mM potassium. We suggest that a voltage‐sensitive chloride channel mediates this continuation of cell swelling. This mechanism may be important in the persistent swelling of astrocytes observed in pathologic conditions such as trauma and seizures where extracellular potassium is elevated, or when other factors are present which may cause astroglial depolarization. © 1995 Wiley‐Liss, Inc.
Characterization and localization of the BM88 antigen in the developing and adult rat brain
Authors: Patsavoudi E. , Merkouri E. , Thomaidou D. , Sandillon F. , Alonso G. , Matsas R. 
Published: January 2005

AbstractMonoclonal antibody BM88 identifies a neuron‐specific antigen (BM88 antigen) present in the central and peripheral nervous system of the pig (Patsavoudi et al.: Neuroscience 30:463–478, 1989; J Neurochem 56:782–788, 1991). We have previously shown that the antigen is also expressed by cultured neurons derived from newborn rat brain. In the present study we have used the monoclonal antibody BM88 and a specific polyclonal antibody in order to identify the nature of the cross‐reactive antigen in rat brain and to investigate its expression and cellular localization in the developing and adult rat nervous system. Western blot analysis and immunocytochemistry revealed that the rat BM88 antigen displays very similar biochemical properties with its porcine homologue. It is a neuron‐specific integral membrane protein, apparently not glycosylated, consisting of two 23 kD polypeptide chains. Immunoperoxidase staining demonstrated that the BM88 antigen is widely distributed in the brain of 19‐day‐old rat embryos. At this stage, immunoreactivity was particularly prominent in differentiated cellular areas and developing fiber tracts of the embryonic rat brain, but was also present in the neuroepithelium. A similar wide distribution of the BM88 antigen was observed in the adult rat brain. Here, immunoreactivity was detected in the neuropil and neuronal perikarya. Immunocytochemical analysis of the expression of the BM88 antigen during postnatal development of the cerebellar cortex showed that this molecule is particularly concentrated in the Purkinje cells between postnatal days 10 to 15; their somata and developing dendrites were distinctly immunopositive during this period. An agedependent increase in the expression of the BM88 antigen both in brain and in the cerebellum was noted. Electron microscopy confirmed the presence of the BM88 reaction product within the perikarya, axons and dendrites of labeled neurons in the adult brain. The BM88 reaction product was preferentially associated with the limiting membrane of mitochondria, endoplasmic reticulum and small electron‐lucent vesicles, but was also present in the plasma membrane, especially at the level of synaptic densities. Our results show that the BM88 antigen participates in an activity common to all or most neurons, and demonstrate that the expression of this antigen is elevated upon neuronal differentiation and maturation. © 1995 Wiley‐Liss, Inc.
A potential interaction of p75 and trkA NGF receptors revealed by affinity crosslinking and immunoprecipitation
Authors: Huber L. J. , Chao M. V. 
Published: January 2005

AbstractNerve growth factor binds independently to two transmembrane receptors, the p75 neurotrophin receptor and the p140trk (trkA) tyrosine kinase receptor, which are both co‐expressed in the majority of neuronal cells that respond to NGF. Previous findings have suggested that appropriate co‐expression of the two receptors gives rise to high affinity NGF binding sites and increased neurotrophin responsiveness; however, evidence demonstrating a direct interaction between the two receptors in cell lines has been lacking. Here we have utilized affinity crosslinking agents with 125I‐NGF to detect an association of trkA and p75 receptors in embryonic spinal cord and brain tissues enriched in the two receptors. Although multimeric complexes of trkA and p75 were not detected by affinity crosslinking, immunoprecipitation of cross‐linked NGF‐receptor complexes with trk‐specific antibodies resulted in selective immunoprecipitation of crosslinked p75. Our results indicate that the trkA and p75 receptors can potentially interact, and that such an association may be responsible for the generation of high affinity NGF binding sites. © 1995 Wiley‐Liss, Inc.
Bovine opsin gene expression exhibits a late fetal to adult regulatory switch
Authors: DesJardin L. E. , Lockwood M. K. , Hauswirth William W. 
Published: January 2005

AbstractRates of bovine photoreceptor gene transcription, as measured by nuclear run‐on assays, exhibit gene‐specific patterns of regulation. Here we investigate initiation and elongation in nuclear run‐on assays with the use of sarkosyl to further understand the nature of these gene‐specific elements. Opsin transcription, alone among several genes tested, proved sarkosyl‐sensitive. This sensitivity is maximal in adult retinas, with inhibition first detected in mid‐third trimester fetal retinas. Therefore, opsin transcription appears to involve different regulatory elements in adult and fetal retinas, implying a fetal to adult switch in the control of opsin gene expression. Although this regulatory switch is initially activated at a time when the fetal outer nuclear layer of the retina first achieves adult‐like morphology, further maturation of opsin regulation takes place postpartum since levels of sarkosyl sensitivity are almost 5‐fold greater in adult retinas compared to the 7.5 month fetus. We also show that the sarkosyl‐induced reduction of opsin transcripton is not due to prevention of de novo RNA polymerase II initiation in the run‐on reaction, suggesting the detergent alters a positive‐acting, postinitiation component of the transcriptional apparatus. Since levels of opsin transcription with sarkosyl are similar to those of the other visual transduction genes with or without sarkosyl, this detergent‐sensitive transcriptional component appears to account for the singularly high, gene‐specific rate of opsin transcription in retinal photoreceptor cells. © 1995 Wiley‐Liss, Inc.
Analysis of proteoglycan expression in developing chicken brain: Characterization of a heparan sulfate proteoglycan that interacts with the neural cell adhesion molecule
Authors: Burg M. A. , Halfter W. , Cole Gregory J. 
Published: January 2005

AbstractIn the present study we have characterized the major proteoglycans of chick brain, focusing on their pattern of expression in development and on identifying the heparan sulfate proteoglycan (HSPG) that binds to the neural cell adhesion molecule (NCAM). The major chondroitin sulfate proteoglycans (CSPG) are a heterogeneous group of molecules with an average MW of 450 kDa. Protein core analysis reveals multiple protein cores between 100 and 350 k Da, The HSPGs are somewhat smaller, with an average MW of 350 kDa, and the major brain HSPG possesses a 250 kDa protein core. During development the relative percentage of HSPG decreases from approximately 50% of total sulfate‐labeled PG at E6 to 25% by E10. In order to begin to characterize the HSPG that interacts with NCAM, we initially used an antiserum produced against a HSPG which was previously shown to copurify with NCAM (Cole and Burg: Exp Cell Res 182:44‐60, 1989). This antiserum immunoprecipitated a HSPG core protein of 250 kDa, corresponding to the major HSPG of chick brain. We also show that the major brain HSPG binds to a synthetic peptide that encodes the heparan sulfate‐binding domain of NC AM, and that monoclonal antibodies to a recently identified chick retinal HSPG recognize this NCAM‐binding HSPG. This HSPG was immunopurified from E10 chick brain using the 6D2 monoclonal antibody, and has been shown to bind an affinity column containing the heparan sulfate‐binding peptide of NCAM. Consistent with its ability to bind NCAM, we show that the intact 6D2 HSPG inhibits cell adhesion to a HBD peptide substratum, and also binds chick brain cells when employed as a substratum. © 1995 Wiley‐Liss, Inc.
Spontaneously immortalized adult mouse Schwann cells secrete autocrine and paracrine growth‐promoting activities
Authors: Watabe K. , Fukuda T. , Tanaka J. , Honda H. , Toyohara K. , Sakai O. 
Published: January 2005

AbstractWe established spontaneously immortalized Schwann cell lines from long‐term cultures of adult mouse dorsal root ganglia and peripheral nerves. One of the cell lines, designated IMS32, responded to mitogenic stimuli by platelet‐derived growth factor (PDGF)‐BB, acidic and basic fibroblast growth factors (aFGF, bFGF), and transforming growth factors (TGF)‐b̃1 and ‐b̃2, as determined by bromodeoxyuridine (BrdU) incorporation and double immunofluorescence for S100 and BrdU. Furthermore, conditioned media (CM) obtained from IMS32 cells showed mitogenic activity for both IMS32 cells and long‐term cultured Schwann cells. Western blot analysis revealed TGF‐b̃‐like molecule in the CM, and the activity was absorbed with anti‐TGF‐b̃ neutralizing antibody. Reverse transcription followed by polymerase chain reaction (RT‐PCR) of IMS32 RNA revealed that these cells expressed TGF‐b̃1, b̃2, and ‐b̃3 transcripts. When rat pheochromocytoma PC 12 cells were incubated with the CM, they developed neurite growth. Coculture of PC12 and IMS32 cells also showed neurite growth of PC12 cells. RNA transcripts of nerve growth factor (NGF), brain‐derived neurotrophic factor (BDNF), neurotrophin‐3 (NT3), ciliary neurotrophic factor (CNTF), and glial cell line‐derived neurotrophic factor (GDNF) were detected from IMS32 cells by RT‐PCR. In these, we sequenced the mouse GDNF cDNA coding region and observed 97% and 90% homologies to corresponding rat and human cDNA sequences, respectively. These results indicate that the immortalized Schwann cell line mitotically responds to various growth factors and secretes autocrine and paracrine growth‐promoting activities in vitro. © 1995 Wiley‐Liss, Inc.
Protein kinase C modulates exogenous acetylcholine current in Xenopus oocytes
Authors: Mileo A. M. , Palma E. , Polenzani L. , Limatola C. , Grassi F. , Eusebi F. 
Published: January 2005

AbstractThe modulation of acetylcholine‐activated current (IACh) by protein kinase C (PKC) was studied in Xenopus laevis oocytes microinjected with either mRNA extracted from C2C12 myotubes (C2C12 mRNA) or RNAs encoding murine αβγδ subunits of the nicotinic ACh receptor (nAChR). Voltage‐clamped oocytes were treated for 90 sec with 12‐0‐tetradecanoylphorbol‐13‐acetate (TPA, 300 nM), a potent PKC activator. Transient increase in the amplitude and acceleration in the decay of IACh were invariably observed within minutes of TPA application, and were independent of extracellular Ca2+ concentration. Both parameters recovered to control within 20–30 min; then a slight depression of IACh developed. By this time, an initial PKC down regulation was observed. At the peak of TPA‐induced potentiation, dose‐response relations suggested an increased binding affinity of nAChR for the neurotransmitter. 4a‐phorbol 12,13‐didecanoate (300 nM), a biologically inactive analogue of TPA, did not affect IACh, while staurosporine (5–10 μM), a potent inhibitor of PKC activity, suppressed the action of TPA on IACh. In oocytes co‐injected with C2C12 mRNA and with rat brain mRNA, IACh was potentiated by 5‐hydroxytryptamine (10 μM), whose receptors are coupled to phosphoinositide hydrolysis. The nAChR‐channel activity in cell‐attached patches increased when TPA was applied to the oocytes. In 50% of the oocytes examined, a sustained depression of the single channel activity followed. We conclude that in Xenopus oocytes an endogenous PKC system regulates the function of embryonic‐type muscle nAChRs. © 1995 Wiley‐Liss, Inc.
Platelet‐derived growth factor is a survival factor for PSA‐NCAM + oligodendrocyte pre‐progenitor cells
Authors: Grinspan J. B. , Franceschini B. 
Published: January 2005

AbstractMature oligodendroglia, which synthesize and express lipids and proteins characteristic of myelin, are generated from precursor cells which are formed in germinal matrix, then migrate widely through the neuraxis. We now demonstrate that these precursor cells can be recognized at a very early stage by their surface expression of polysialylated neural cell adhesion molecules (PSA‐NCAM), and only later bind anti ganglioside antibodies that had previously been used to recognize “O‐2A” oligodendroglial precursor cells. PSA‐NCAM expression by these cells is likely to be of functional significance, since a recent study demonstrated that O‐2A cells become immobile when stripped of PSA‐NCAM. Platelet‐derived growth factor (PDGF) proved to be a survival factor for these PSA‐NCAM + cells, and in a defined medium, PDGF was sufficient to ensure maturation of immunopurified PSA‐NCAM + cells to oligodendroglia. © 1995 Wiley‐Liss, Inc.
Differential expression of exons 10 and 11 in normal tau and tau associated with paired helical filaments
Authors: Ksiezak‐Reding H. , Shafit‐Zagardo B. , Yen S.‐H. 
Published: January 2005

AbstractAntibodies were raised to two synthetic peptides with amino acid sequences encoded by a variable region of exons 10 and 11 of the tau gene. The affinity‐purified antibodies, designated E‐10 and E‐11, were used to determine whether PHF‐tau and normal tau differ in variants containing three or four repeats in the microtubule‐binding domain, respectively. Normal adult human brain was shown by gel electrophoresis to contain six isoforms of tau. All of the isoforms reacted with E‐11, whereas only four of them with slower electrophoretic mobility were recognized by E‐10. Fetal brain tau was readily recognized by E‐11 but reacted poorly with E‐10. In PHF preparations, E‐11 bound to all three polypeptides of PHF‐tau of 68 kD, 64 kD, and 60 kD and reacted intensely with a material smearing from the top of the gel to about the 50‐kD region. In contrast, E‐10 only weakly recognized the two higher molecular weight PHF‐tau polypeptides of 68 kD and 64 kD, as well as smeared material, and the binding was not affected by phosphatase treatment. Using recombinant tau with four repeats as a reference, the immunoreactivity of E‐10 with PHF‐tau was estimated to be approximately 5% of that of E‐11. By comparison, the immunoreactivity of E‐10 with four isoforms of normal tau was comparable to that of E‐11. These results indicate that the ratio of three vs. four repeat variants in PHF‐tau is higher than in normal tau and suggest that Alzheimer disease may be associated with the disproportional expression of fetal (or juvenile) forms of tau. Alternatively, the weak reactivity of PHF‐tau with E‐10 antibody could be due to post‐translational modifications other than phosphorylation. © 1995 Wiley‐Liss, Inc.