bluuebunny/crossref_metadata_2025_split huggingface dataset:
Alterations in Actin‐Binding β‐Thymosin Expression Accompany Neuronal Differentiation and Migration in Rat Cerebellum
Authors: Border Barbara G. , Lin Sheng‐Cai , Griffin W. Sue T. , Pardue Sibile , Morrison‐Bogorad Marcelle 
Published: October 2006

AbstractThe β4‐and β10‐thymosins, recently identified as actin monomer‐sequestering proteins, are developmentally regulated in brain. Using specific mRNA and protein probes, we have used in situ hybridization and immunohis‐tochemical techniques to investigate the distribution of the β‐thymosin mRNAs and their proteins in developing rat cerebellum. Early in postnatal development, both β‐thymosin mRNAs were expressed at highest levels in the postmitotic, premigratory granule cells of the external granular layer; expression diminished as granule cells migrated to and differentiated within the developing internal granular layer. In addition, both β‐thymosin proteins were present in bundles of cerebellar afferent fibers in the white matter at this time. Throughout the maturation period, both proteins were present in elongating parallel fibers in the upper portion of the molecular layer. Later in cerebellar development, thymosin β4, but not thymosin β10, was expressed in Golgi epithelial cells and Bergmann processes. Thymosin β4 was expressed in a small population of cells with microglial morphology scattered throughout the gray and white matter. Thymosin β10 was detected in an even smaller population of glia. Expression of thymosin β4 and thymosin β10 in premigratory granule cells and in growing neuronal processes is consistent with the possibility that both β‐thymosins are involved in the dynamics of actin polymerization during migration and process extension of neurons.
A Neurofilament‐Associated Kinase Phosphorylates Only a Subset of Sites in the Tail of Chicken Midsize Neurofilament Protein
Authors: Hollander Brian A. , Ayyub Champakali , Shaw Gerry , Bennett Gudrun S. 
Published: October 2006

AbstractAlthough neurofilaments are among the most highly phosphorylated proteins extant, relatively little is known about the kinases involved in their phosphorylation. The majority of the phosphates present on the two higher‐molecular‐mass neurofilament subunits are added to multiply repeated sequence motifs in the tail. We have examined the specificity of a neurofilament‐associated kinase (NFAK) partially purified from chicken spinal cord that selectively phosphorylates the middle‐molecular‐mass neurofilament subunit, NF‐M. Two‐dimensional phosphopeptide mapping of 32P‐labeled NF‐M shows that, in vitro, NFAK phosphorylates a subset of peptides phosphorylated in vivo in cultured neurons. The absence of a complete complement of labeled phosphopeptides following in vitro phosphorylation, compared with phosphorylation in vivo, is not due to a lack of availability of phosphorylation sites because the same maps are obtained when enzymatically dephosphorylated NF‐M is used as an in vitro substrate. Phosphopeptide maps from in vitro‐phosphorylated NF‐M and those from a recombinant fusion protein containing only a segment of the tail piece of chicken NF‐M reveal identical labeled peptides. The fusion protein lacks a segment containing 17 KXX(S/T)P putative phosphorylation sites contained in the tail of chicken NF‐M but contains a segment that includes four KSPs and a KSD site also present in the intact tail. These results suggest (a) that NFAK mediates the phosphorylation of some, but not all, potential phosphorylation sites within the tail of NF‐M and (b) that multiple kinases are necessary for complete phosphorylation of the NF‐M tail.
Growth Conditions Differentially Regulate the Expression of α‐Amino‐3‐Hydroxy‐5‐Methylisoxazole‐4‐Propionate (AMPA) Receptor Subunits in Cultured Neurons
Authors: Condorelli D. F. , Dell'Albani P. , Aronica E. , Genazzani A. A. , Casabona G. , Corsaro M. , Balazs R. , Nicoletti F. 
Published: October 2006

AbstractWe have studied the expression of a‐amino‐3‐hydroxy‐5‐methylisoxazole‐4‐propionate (AMPA) receptor subunits in cultured cerebellar granule cells [7 days in vitro (DIV)] grown in medium containing different concentrations of K± (10, 25, or 40 mM) with or without 100 μM N‐methyl‐D‐aspartate (NMDA; added once after 2 DIV). All these conditions are known to influence maturation and survival of granule cells, as well as the functional expression of NMDA receptors during development in culture. The expression of both glutamate receptor (GluR) subunit 1 mRNA and receptor protein was low in cultures grown in 10 mM K± (K10) and increased dramatically in cultures grown in 25 mM K± (K25), with intermediate levels found in cultures grown in K10 and chronically exposed to NMDA (K10 ± NMDA). In cultures grown in 40 mM K± (K40), the expression of GluR1 mRNA and receptor protein was lower than in K25 but still higher than in K10. GluR2 and ‐3 subunits were differently regulated by growth conditions, with their expression being higher in K10 and progressively reduced to the lowest levels in K40 (both mRNA and receptor proteins). GluR4 mRNA levels did not differ between K10 and K25, although they were reduced by chronic exposure to NMDA. To test how the differential expression of the various subunits affects the functional activity of AMPA receptors, we have measured AMPA‐stimulated 4SCa2± influx and 40‐[3H]phorbol 12, 13‐dibutyrate binding in intact cells. Both functional parameters increased along with the K± concentration and were maximal in K40, in coincidence with the lowest expression of the GluR2 subunits. These results indicate that functional diversity of AMPA receptors can be generated by the degree of chronic depolarization and/or exposure to NMDA in neurons developing in primary culture.
Neither Moderate Hypoxia nor Mild Hypoglycaemia Alone Causes Any Significant Increase in Cerebral [Ca2±i: Only a Combination of the Two Insults Has This Effect.: A 31P and 19F NMR Study
Authors: Badar‐Goffer Ronnitte S. , Thatcher Nicola M. , Morris Peter G. , Bachelard Herman S. 
Published: October 2006

Abstract(1) The energy state and free intracellular calcium concentration ([Ca2±i) of super‐fused cortical slices were measured in moderate hypoxia (∼65 μM O2), in mild hypoglycaemia (0.5 mM glucose), and in combinations of the two insults using 19F and 31P NMR spectroscopy. (2) Neither hypoxia nor hypoglycaemia alone caused any significant change in [Ca2±i. Hypoxia caused a 40% fall in phosphocreatine (PCr) content but not in ATP level, and hypoglycaemia produced a slight fall in both (as expected from previous studies). These changes in the energy state recovered on return to control conditions. (3) A combined sequential insult (hypoxia, followed by hypoxia plus hypoglycaemia) produced a 100% increase in [Ca2±, and a decrease in PCr level to ∼25% of control. The reverse combined sequential insult (hypoglycaemia, followed by hypoglycaemia plus hypoxia) had the same effect. On return to control conditions there was some decrease in [Ca2±i and a small increase in PCr content, but neither recovered to control levels. (4) Exposure of the tissue to the combined simultaneous insult (hypoxia plus hypoglycaemia) immediately after the control spectra had been recorded resulted in a fivefold increase in [Ca2±i and a similar decrease in PCr level to 20–25% of control. There was little if any change of [Ca2±i or PCr level on return to control conditions. (5) These results are discussed in terms of metabolic adaptation of some but not all of the cortical cells to the single type of insult, which renders the tissues less vulnerable to the combined insult.
Chicken Tyrosine Hydroxylase Gene: Isolation and Functional Characterization of the 5′ Flanking Region
Authors: Carrier Alice , Devignes Marie‐Dominique , Renoir Dominique , Auffray Charles 
Published: October 2006

AbstractTyrosine hydroxylase (TH) is the rate‐limiting enzyme in the biosynthesis of catecholamines. We describe here the isolation of the chicken TH gene and the analysis of 3 kb of its 5′ flanking region. The chicken TH transcription unit spans 19 kb. The 60‐bp proximal promoter contains a TATA box and a cyclic AMP response element (CRE) sequence. The 5′ flanking region contains several AP1‐, AP2‐, and octamer‐like sequences as well as a glucocorticoid response element at position ‐1.4 kb. A construct containing the 3‐kb 5′ flanking DNA fused to the chloramphenicol acetyltransferase (CAT) gene was transiently transfected into PC12 cells, and the effect of various effectors was tested. Only forskolin increased the CAT activity, likely owing to the presence of the CRE sequence. Constructs prepared by progressively deleting the 5′ flanking DNA were transfected into PC12 and QT6 (quail transformed fibroblasts) cells. In both cell types, the transcriptional activity increased with deletion of the 5′ flanking region. These results show that the 60‐bp region containing the TATA box and the CRE is sufficient to act as a constitutive promoter for the chicken TH gene and that this region appears to be negatively controlled by upstream sequences.
A Previous Potassium Stimulation Enhances the Increases of Striatal Extracellular Dopamine and 5‐Hydroxytryptamine During Global Ischaemia Under Simulated Penumbral Conditions
Authors: Richards D. A. , Obrenoyitch T. P. , Johonson‐Mora A. , Mase M. , Symon L. , Curzon G. 
Published: October 2006

AbstractThe effect of a previous K± stimulation on striatal extracellular monoamine levels during global ischaemia, under simulated penumbral conditions, was investigated. Rats were implanted with microdialysis probes in both striata, monoamine release was stimulated unilaterally by adding K± (100 mM, 20 min) to the artificial CSF perfused through one probe, and bilateral partial ischaemia was imposed after monoamine levels had returned to basal values or below. Resultant increases in dialysate levels of dopamine and 5‐hydroxytryptamine were markedly and significantly greater on the side previously exposed to K±, even though electrophysiological measurements indicated similarly severe ischaemia on both sides. Associated monoamine metabolite changes did not differ significantly between the two sides. There was no evidence of greater neuronal loss in the K±‐stimulated striata 7 days after ischaemia. However, striatal tissue probably exposed to the highest concentrations of K± could not be examined because of extensive gliosis around the probe.
ucb 11056, a New Potential Nootropic Drug, Amplifies Induced Cyclic AMP Formation in Rat Brain Tissue
Authors: Tamer A. El , Raikoff K. , Corey J. , Wulfert E. , Hanin I. 
Published: October 2006

Abstractucb 11056 [2‐(4‐morpholino‐6‐propyl‐1, 3, 5‐triazin‐2‐yl)aminoethanol] induced a significant (∼25%) increase in cyclic AMP levels in different brain areas following its intraperitoneal injection. This effect started as early as 2 min postinjection and lasted for 30 min, after which cyclic AMP levels returned to normal. In hippocampal slice preparations in vitro, ucb 11056 exerted a strong potentiation of cyclic AMP levels when it was combined with agents such as norepinephrine, forskolin, and isoproterenol. Only a slight effect on cyclic AMP levels was measured when ucb 11056 was incubated alone with hippocampal slices. The potentiating effect of ucb 11056 on norepinephrine‐stimulated cyclic AMP formation was partially reduced when slices were pretreated with yohimbine and totally abolished when slices were treated with propranolol. These combined data indicate that (a) ucb 11056 rapidly increases cyclic AMP levels in the rat brain in vivo and (b) ucb 11056 potentiates stimulated cyclic AMP formation in vitro. The data also suggest that the central effect of ucb 11056 might be via the modulation of cyclic AMP generation, most probably mediated through adenylate cyclase activation mechanisms combined with a weak inhibitory activity on the cyclic nucleotide phosphodiesterase activity.
Clearance of Exogenous Dopamine in Rat Dorsal Striatum and Nucleus Accumbens: Role of Metabolism and Effects of Locally Applied Uptake Inhibitors
Authors: Cass Wayne A. , Zahniser Nancy R. , Flach Karen A. , Gerhardt Greg A. 
Published: October 2006

AbstractIn vivo electrochemistry was used to investigate the mechanisms contributing to the clearance of locally applied dopamine in the dorsal striatum and nucleus accumbens of urethane‐anesthetized rats. Chronoamperometric recordings were continuously made at 5 Hz using Nafion‐coated carbon fiber electrodes. When a finite amount of dopamine was pressure‐ejected at 5‐min intervals from a micropipette adjacent to the electrode, transient and reproducible dopamine signals were detected. Substitution of L‐a‐methyldopamine, a substrate for the dopamine transporter but not for monoamine oxidase, for dopamine in the micropipette did not substantially alter the time course of the resulting signals. This indicates that metabolism of locally applied dopamine to 3,4‐dihydroxyphenylacetic acid is not responsible for the decline in the dopamine signal. Similarly, changing the applied oxidation potential from ±0.45 to ±0.80 V, which allows for detection of 3‐methoxytyramine formed from dopamine via catechol‐O‐methyltransferase, had little effect on signal amplitude or time course. In contrast, lesioning the dopamine terminals with 6‐hydroxydopamine, or locally applying the dopamine uptake inhibitors cocaine or nomifensine before pressure ejection of dopamine, significantly increased the amplitude and time course of the dopamine signals in both regions. The effects of cocaine and nomifensine were greater in the nucleus accumbens than in the dorsal striatum. Local application of lidocaine and procaine had no effect on the dopamine signals. Initial attempts at modeling resulted in curves that were in qualitative agreement with our experimental findings. Taken together, these data indicate that (1) uptake of dopamine by the neuronal dopamine transporter, rather than metabolism or diffusion, is the major mechanism for clearing locally applied dopamine from the extracellular milieu of the dorsal striatum and nucleus accumbens, and (2) the nucleus accumbens is more sensitive to the effects of inhibitors of dopamine uptake than is the dorsal striatum.
Ceramide 1‐Phosphate Phosphatase Activity in Brain
Authors: Shinghal Rajesh , Scheller Richard H. , Bajjalieh Sandra M. 
Published: October 2006

AbstractRecent studies have implicated sphingolipids in a variety of intracellular signaling systems. The finding that a calcium‐stimulated ceramide kinase copurifies with neurotransmitter‐containing vesicles suggests that ceramide, or one of its metabolites, has a role in neurotransmitter release. As a step toward understanding the role of ceramide kinase in vesicle functioning, this study sought to determine the metabolic fate of the product, ceramide 1‐phosphate. We report that ceramide 1‐phosphate is not deacylated by brain ceramidases to produce sphingosine 1‐phosphate. It is, however, the substrate for a phosphatase activity that we name ceramide 1‐phosphate phosphatase (CPPase). Subcellular fractionation studies suggest that CPPase is found in the synaptic terminal and is associated with both synaptic vesicle and plasma membranes. Divalent cations, most notably calcium, inhibit CPPase activity although not at concentrations that activate ceramide kinase. The existence of both ceramide kinase and CPPase activities at the synapse suggests that ceramide 1‐phosphate production regulates some aspect of synaptic vesicle functioning.
NMDA and AMPA Receptors in Transgenic Mice Expressing Human β‐Amyloid Protein
Authors: Sandhu Faheem A. , Porter Richard H. P. , Eller Robert V. , Zain Sayeeda B. , Salim Mohammad , Greenamyre J. Timothy 
Published: October 2006

AbstractThe human β‐amyloid protein may play an important, possibly primary, role in the pathogenesis of Alzheimer's disease (AD), and it appears to potentiate the susceptibility of neurons to excitotoxicity. AD is associated with alterations in the W‐methyl‐D‐aspartate (NMDA) and a‐amino‐3‐hydroxy‐5‐methylisoxazole‐4‐proprionic acid (AMPA) subtypes of glutamate receptors, and it has been suggested that excitotoxicity may play a role in neuronal damage in AD. In this study, we have used quantitative receptor autoradiography to examine NMDA and AMPA receptors in transgenic mice that contain the gene for the carboxyl‐terminal 100 amino acids of the human amyloid precursor protein, beginning with the β‐amyloid region, which is under the control of the JC viral early region promoter. Reverse transcriptase‐polymerase chain reaction confirmed that the brains of transgenic mice expressed β‐amyloid mRNA and that control mice did not. NMDA receptors, assessed with [3H]MK‐801, were unchanged in the transgenic compared with the control mice. In the transgenic mice, there were no significant changes in [3H]AMPA receptor binding compared with controls. This study represents the first attempt to evaluate in transgenic mice the in vivo interaction between β‐amyloid expression and excitatory amino acid receptors.
Expression of the Baculovirus p35 Gene Inhibits Mammalian Neural Cell Death
Authors: Rabizadeh S. , LaCount D. J. , Friesen P. D. , Bredesen D. E. 
Published: October 2006

AbstractExpression of the apoptosis suppressor genep35, derived from the baculovirus Autographa californica nuclear polyhedrosis virus, markedly inhibited the cell death of stably transfected mammalian neural cells whether the cell death was induced by glucose withdrawal, calcium ionophore, or serum withdrawal. The p35 protein, which is required to block virus‐induced apoptosis of cultured insect cells, is only the second gene product shown to block mammalian neural cell death, with Bcl‐2 being the first. Because there is no apparent homology between p35 and Bcl‐2, the existence of a cellular death program that may be modulated at multiple points is suggested/Furthermore, these findings demonstrate that the putative cellular death program is conserved across species and cell types.
Superoxide Dismutase Activity, Oxidative Damage, and Mitochondrial Energy Metabolism in Familial and Sporadic Amyotrophic Lateral Sclerosis
Authors: Bowling Allen C. , Schulz Jorg B. , Brown Robert H. , Beal M. Flint 
Published: October 2006

AbstractThe cause of neuronal death in amyotrophic lateral sclerosis (ALS) is unknown. Recently, it was found that some patients with autosomal‐dominant familial ALS (FALS) have point mutations in the gene that encodes Cu/Zn superoxide dismutase (SOD1). In this study of postmortem brain tissue, we examined SOD activity and quantified protein carbonyl groups, a marker of oxidative damage, in samples of frontal cortex (Brodmann area 6) from 10 control patients, three FALS patients with known SOD1 mutations (FALS‐1), one autosomal‐dominant FALS patient with no identifiable SOD1 mutations (FALS‐0), and 11 sporadic ALS (SALS) patients. Also, we determined the activities of components of the electron transport chain (complexes I, II‐III, and IV) in these samples. The cytosolic SOD activity, which is primarily SOD1 activity, was reduced by 38.8% (p < 0.05) in the FALS‐1 patients and not significantly altered in the SALS patients or the FALS‐0 patient relative to the control patients. The mitochondrial SOD activity, which is primarily SOD2 activity, was not significantly altered in the FALS‐1, FALS‐0, or SALS patients. The protein carbonyl content was elevated by 84.8% (p < 0.01) in the SALS patients relative to the control patients. Finally, the complex I activity was increased by 55.3% (p < 0.001) in the FALS‐1 patients relative to the control patients. These results from cortical tissue demonstrate that SOD1 activity is reduced and complex I activity is increased in FALS‐1 patients and that oxidative damage to proteins is increased in SALS patients.
Botulinum A Like Type B and Tetanus Toxins Fulfils Criteria for Being a Zinc‐Dependent Protease
Authors: Paiva Anton de , Ashton Anthony C. , Foran Patrick , Schiavo Giampetro , Montecucco Cesare , Dolly J. Oliver 
Published: October 2006

AbstractAlthough botulinum neurotoxin (BoNT) types A and B and tetanus toxin (TeTx) are specific inhibitors of transmitter release whose light chains contain a zinc‐binding motif characteristic of metalloendoproteases, only the latter two proteolyse synaptobrevin. Chelation of zinc or its readdition at high concentration hindered blockade of neuromuscular transmission by BoNT/A and B, indicating that type A also acts via a zinc‐dependent mechanism. Such treatments prevented proteolysis of synaptobrevin II in rat brain synaptic vesicles by BoNT/B and TeTx but only the activity of the latter was antagonised appreciably by ASQFETS, a peptide spanning their cleavage site. The toxins’ neuroparalytic activities were attenuated by phosphoramidon or captopril, inhibitors of certain zinc requiring proteases. However, these agents were ineffective in reducing the toxins’ degradation of synaptobrevin except that a high concentration of captopril partially blocked the activity of TeTx but not BoNT/B, as also found for these drugs when tested on synaptosomal noradrenaline release. These various criteria establish that a zinc‐dependent protease activity underlies the neurotoxicity of BoNT/A, a finding confirmed at motor nerve endings for type B and TeTx. Moreover, the low potencies of captopril and phosphoramidon in counteracting the toxins’ effects necessitate the design of improved inhibitors for possible use in the clinical treatment of tetanus or botulism.
Domain Poisoning: The Redundancy of Current Models of Assessment through Art
Authors: Hardy Tom 
Published: October 2006

AbstractWith the National Foundation for Educational Research concluding that schools which include Contemporary Art Practice (CAP) in their curriculum add significant value to their students' art experience, [1] and at a time when much of the discussion around contemporary art questions the value of the art object itself, this article addresses the question: how are we to engage students with the contemporary and, at the same time, make value judgments of their own work?And, while the professional fine art world subscribes increasingly to the ‘rhizomatic’ [2] template of art processes, how do we square this with current assessment criteria which require that students produce work where the preparation and finished product occupy separate domains and rely on ‘procedures and practices that reach back to the nineteenth century’? [3] By way of a postscript to the inconclusive findings of the Eppi‐centre art and design review group [4], this article will also address what we have lost in the drive for domain‐based assessment and how to regain some of the ground lost since the introduction of Curriculum 2000.
Art Education and the Visual Arts in Botswana
Authors: Brennan Geraldine 
Published: October 2006

AbstractThe history of art and design education in Botswana has evolved in a unique way and reflects its British colonial history and post‐independence development. It has involved constant exchange and dialogue with other countries through the employment of teachers, teacher trainers and university lecturers from a variety of European, Asian and other African countries. This dialogue has continued as locally trained art teachers pursue their degrees overseas and return with new ideas and influences. At the same time, the development of local crafts for a global market and the inter‐cultural exchange in the visual arts outside the formal education system are thriving with the help of various organisations and the museum and gallery sector.This article will look more closely at the country context, the history and development of art education and the interrelationships that have evolved over the last two decades. It will show how students engage with the challenge of integrating their African heritage and changing traditions with their development as teachers and artists. It will also consider how closer links between the formal and informal art sectors might be mutually beneficial and demonstrate the potential for art and design to play a role in the social, economic and cultural development of the country.