bluuebunny/crossref_metadata_2025_split huggingface dataset:
Stabilization of thalamo‐cortical long‐term potentiation by the amygdala: cholinergic and transcription‐dependent mechanisms
Authors: Dringenberg Hans C. , Kuo Min‐Ching , Tomaszek Summer 
Published: July 2004

AbstractSynaptic potentiation allows neurons to enhance excitability and store information for extended time periods. We examined the role of the amygdaloid complex, known to facilitate long‐term memory encoding, to influence synaptic strength at thalamo‐cortical synapses. In urethane‐anaesthetized rats, theta‐burst stimulation of the dorsal lateral geniculate nucleus of the thalamus induced early phase (1–2 h) long‐term potentiation (LTP) of the field postsynaptic potential (fPSP) recorded in the ipsilateral primary visual cortex. Electrical stimulation (100 Hz) of the amygdala 5 min after thalamic stimulation converted early phase LTP to stable late‐phase (> 4 h) LTP. This effect was not correlated with the degree of electrocorticographic activation of V1 induced by amygdala stimulation. Amygdala stimulation without thalamic theta‐burst stimulation did not change thalamo‐cortical fPSPs. The centrally acting cholinergic‐muscarinic receptor antagonist scopolamine (1 mg/kg, i.p.), but not peripherally acting methyl‐scopolamine, completely blocked the amygdala‐induced conversion of early to late‐phase thalamo‐cortical LTP. Further, ventricular application of the transcription inhibitor anisomycin (250 µg) reduced amygdala‐induced late‐phase LTP induction. These results demonstrate that the amygdaloid complex transforms time‐limited synaptic enhancement of thalamo‐cortical transmission into long lasting increases in synaptic strength. These processes are mediated, at least in part, by cholinergic and transcription‐dependent mechanisms. These amygdaloid‐induced effects provide a potential mechanism underlying long‐term enhancement of sensory transmission and information encoding in thalamo‐cortical networks.
Debt, Growth and Budgetary Regimes
Authors: Ghosh Sugata , Mourmouras Iannis A. 
Published: July 2004

AbstractWithin the Barro (1990) model of productive public services, but with the inclusion of public debt, we derive and characterize on the balanced growth path, a set of welfare‐maximizing fiscal rules under two budgetary regimes – one with only the standard dynamic government budget constraint, and the other involving the golden rule of public finance. We demonstrate analytically that the optimal fiscal policy differs in the two budgetary regimes considered. We also analyse two cases within the second regime: one, where the ratio of current spending to tax revenues is parametrically given, and another, where this ratio is optimally chosen by the government.
Inflation, Shadow Prices and the EMU: Evidence From Greece
Authors: Tsionas Efthymios G. , Christopoulos Dimitris K. 
Published: July 2004

AbstractThe paper examines whether inflation systematically distorts the informational content of price signals. A shadow cost function is specified, and the deviation of shadow from actual prices is modeled as a function of the level of economy‐wide inflation, as well as other conditioning variables like budget deficits and changes in inflation rate. It is found that inflation is associated with significant allocative costs in most Greek manufacturing sectors. Measures of cost gains resulting from Greece's convergence towards the EMU are provided and the policy implications are explored.
Folk Theorem For Bilateral Bargaining with Vector Endowments
Authors: Horniacek Milan 
Published: July 2004

AbstractWe analyse a bargaining game of two players on the division of the sum of their vector endowments, with alternating proposals and discounting of single period utilities. The pair of endowments is not weakly Pareto‐efficient. Until they reach an agreement, each of the parties can withdraw from bargaining and keep their endowments. Any strictly individually rational division of the sum of endowments can emerge in some subgame perfect equilibrium if discount factors are close enough to one. Each subgame perfect equilibrium, in which the parties’ decisions do not depend on past rejected proposals, leads to a weakly Pareto‐efficient agreement in the first period.
From biography to history: writing the modern British monarchy
Authors: Cannadine David 
Published: July 2004

Abstract
This article traces the development of biographical and historical writing about the British monarchy from the ‘golden age’ of Elizabeth I to the House of Windsor. It examines the differences in approach over the past two centuries, in particular, from the uncritical biographies of the Victorian period to the current unregulated flood of material, authorized and unauthorized. Such an analysis goes beyond the history of dynasties and individuals and becomes a history of society as reflected in the changing experiences of the British royal family.
The household and entourage of Charles I of Anjou, king of the Regno, 1266–85
Authors: Dunbabin Jean H. 
Published: July 2004

Abstract
This article attempts to reconstitute from the scrappy surviving records Charles I's household and court. For a conqueror, the choice of companions could have serious political implications. While Charles's immediate domestic circle was French in origin and organized on the example of Louis IX's household, he deliberately encouraged and paid for the attendance of men from Provence and the Regno, both in his travelling entourage and at his great court appearances at liturgical feasts. Beyond these intimates, he accepted into his fidelity, and therefore into his broader court circle, a wide range of talented individuals from all parts of his ‘empire’.
Brain to blood efflux transport of adenosine: blood–brain barrier studies in the rat
Authors: Isakovic Aleksandra J. , Abbott N. Joan , Redzic Zoran B. 
Published: July 2004

AbstractThe blood–brain barrier (BBB) efflux transport of [14C] adenosine was studied using the brain efflux index (BEI) technique. BEI increased linearly over the first 2 min after injection, with deviation from linearity thereafter; 90.12 ± 1.5% of the injected [14C] radioactivity remained within the brain after 20 min. The remaining tracer appears to be mainly intracellular, trapped by phosphorylation, as an almost linear increase of BEI over 20 min was observed after intracerebral injection of [14C] adenosine together with 5‐iodo tubercidin. The BBB efflux clearance of [14C] radioactivity was estimated to be 27.62 ± 5.2 µL/min/g, almost threefold higher than the BBB influx clearance estimated by the brain uptake index technique. High‐performance liquid chromatography (HPLC) analysis of blood plasma collected from the jugular vein after the intracerebral injection revealed metabolic breakdown of [14C] adenosine into nucleobases. The BBB efflux transport was saturable with apparent Km = 13.22 ± 1.75 µm and Vmax = 621.07 ± 71.22 pmole/min/g, which indicated that BBB efflux in vivo is 6.2–12p mole/min/g, negligible when compared to the reported rate of adenosine uptake into neurones/glia. However, these kinetic parameters also suggest that under conditions of elevated ISF adenosine in hypoxia/ischaemia, BBB efflux transport could increase up to 25% of the uptake into neurones/glia and become an important mechanism to oppose the rise in ISF concentration. HPLC‐fluorometry detected 93.6 ± 5.25 nm of adenosine in rat plasma, which is 17‐ to 220‐fold lower than the reported Km of adenosine BBB influx in rat. Together with the observed rapid degradation inside endothelial cells, this indicated negligible BBB influx of intact adenosine under resting conditions. Cross‐inhibition studies showed that unlabelled inosine, adenine and hypoxanthine caused a decrease in BBB efflux of [14C] radioactivity in a concentration‐dependent manner, with Ki of 16.7 ± 4.88, 65.1 ± 14.1 and 71.1 ± 16.9 µm, respectively. This could be due to either competition of unlabelled molecules with [14C] adenosine or competition with its metabolites hypoxanthine and adenine for the same transport sites.
Phosphorylation of microtubule‐associated protein tau by isoforms of c‐Jun N‐terminal kinase (JNK)
Authors: Yoshida Hirotaka , Hastie C. James , McLauchlan Hilary , Cohen Philip , Goedert Michel 
Published: July 2004

AbstractMicrotubule‐associated protein tau in a hyperphosphorylated state is the major component of the filamentous lesions that define a number of neurodegenerative diseases commonly referred to as tauopathies. Hyperphosphorylation of tau at most sites appears to precede filament assembly. Many of the hyperphosphorylated sites are serine/threonine–proline sequences. Here we show that c‐Jun N‐terminal kinases JNK1, JNK2 and JNK3 phosphorylate tau at many serine/threonine–prolines, as assessed by the generation of the epitopes of phosphorylation‐dependent anti‐tau antibodies. Of the three protein kinases, JNK2 phosphorylated the most sites in tau, followed by JNK3 and JNK1. Phosphorylation by JNK isoforms resulted in a greatly reduced ability of tau to promote microtubule assembly. These findings extend the number of candidate protein kinases for the hyperphosphorylation of tau in Alzheimer's disease and other neurodegenerative disorders.
HIF‐1α reveals a binding activity to the promoter of iNOS gene after permanent middle cerebral artery occlusion
Authors: Matrone C. , Pignataro G. , Molinaro P. , Irace C. , Scorziello A. , Di Renzo G. F. , Annunziato L. 
Published: July 2004

AbstractHypoxia inducible factor (HIF‐1)‐1α is a specific, oxygen‐sensitive protein that regulates the activity of HIF‐1, a transcriptional factor that increases after cerebral ischemia and may either promote or prevent neuronal survival. In this study to determine whether the inducible nitric oxide synthase (iNOS) gene containing the sequence of the hypoxia‐responsive enhancer (HRE) was an HIF‐1 target after cerebral ischemia induced by permanent middle cerebral artery occlusion (pMCAO), electrophoretic mobility shift assay (EMSA) and iNOS western blot analysis were performed in the ischemic core, in the area surrounding the infarct and in the hippocampus ipsilateral and contralateral to the lesion. In addition, both HIF‐1α mRNA and protein expression were examined in the ischemic core, in the area surrounding the ischemic core and in the hippocampus ipsilateral to the insult. Our results revealed that pMCAO up‐regulates iNOS protein in the ischemic core, in the area surrounding the ischemic core and in the hippocampus ipsilateral to the lesion, and that the activation of iNOS expression is mediated by HIF‐1. Moreover, HIF‐1α mRNA and protein levels increased in the ischemic core and in the hippocampus ipsilateral to the lesion compared with the levels obtained in the corresponding areas of sham‐operated controls or in the contralateral hemisphere. Particularly in the area surrounding the ischemic core, HIF‐1α protein accumulated during pMCAO although mRNA did not increase. Our study suggests that the activation of HIF‐1 might be involved in the mechanisms whereby iNOS promotes cell survival and/or death after cerebral ischemia.
Stimulus‐dependent regulation and cellular expression of genes encoding neuropeptides, prohormone convertases, α‐amidating enzyme and 7B2 in identified Lymnaea neurons
Authors: Spijker Sabine , Sharp‐Baker Hilary E. , Geraerts Wijnand P. M. , Van Minnen Jan , Smit August B. 
Published: July 2004

AbstractSynthesis of bioactive peptides is regulated by several post‐translational processing events, including cleavage of peptides from a prohormone, and chemical modifications. Using quantitative in situ hybridization and neuron‐specific macro‐arrays, we first demonstrated cell‐type specific expression levels of transcripts encoding prohormone convertases, peptide α‐amidating enzyme as well as the chaperone 7B2 in Lymnaea neurons. Second, we demonstrated a strict correlation between α‐amidating enzyme and its neuropeptide substrates. However, this strict relationship of gene expression of the three prohormone convertases and types of cleavage site used is not present. Third, we showed by a physiological stimulus, i.e. clean water, which leads to a stereotyped egg‐laying behaviour resulting in successful egg‐mass deposition, the co‐regulated induction of transcript levels of processing enzymes, 7B2, and egg‐laying hormone. These data indicate that (i) these enzymes (and chaperone) are involved in egg‐laying hormone neuropeptide biosynthesis, and (ii) neuropeptide release and transcript levels of both prohormones and processing enzymes are regulated in accordance with physiological demands.
UCH‐L1 aggresome formation in response to proteasome impairment indicates a role in inclusion formation in Parkinson's disease
Authors: Ardley Helen C. , Scott Gina B. , Rose Stephen A. , Tan Nancy G. S. , Robinson Philip A. 
Published: July 2004

AbstractAggresomes are associated with many neurodegenerative disorders, including Parkinson's disease, and polyglutamine disorders such as Huntington's disease. These inclusions commonly contain ubiquitylated proteins. The stage at which these proteins are ubiquitylated remains unclear. A malfunction of the ubiquitin/proteasome system (UPS) may be associated with their formation. Conversely, it may reflect an unsuccessful attempt by the cell to remove them. Previously, we demonstrated that overexpression of Parkin, a ubiquitin‐protein ligase associated with autosomal recessive juvenile Parkinsonism, generates aggresome‐like inclusions in UPS compromised cells. Mutations in the de‐ubiquitylating enzyme, UCH‐L1, cause a rare form of Parkinsonism. We now demonstrate that overexpression of UCH‐L1 also forms ribbon‐like aggresomes in response to proteasomal inhibition. Disease‐associated mutations, which affect enzymatic activities, significantly increased the number of inclusions. UCH‐L1 aggresomes co‐localized with ubiquitylated proteins, HSP70, γ‐tubulin and, to a lesser extent, the 20S proteasome and the chaperone BiP. Similar to Parkin inclusions, we found UCH‐L1 aggresomes to be surrounded by a tubulin rather than a vimentin cage‐like structure. Furthermore, UCH‐L1 aggregates with Parkin and α‐synuclein in some, but not all inclusions, suggesting the heterogeneous nature of these inclusion bodies. This study provides additional evidence that aggregation‐prone proteins are likely to recruit UPS components in an attempt to clear proteins from failing proteasomes. Furthermore, UCH‐L1 accumulation is likely to play a pathological role in inclusion formation in Parkinson's disease.
CRF receptor type 1 and 2 expression and anatomical distribution in the rat colon
Authors: Chatzaki Ekaterini , Crowe Paul D. , Wang Lixin , Million Mulugeta , Taché Yvette , Grigoriadis Dimitri E. 
Published: July 2004

AbstractCorticotropin‐releasing factor (CRF) receptor agonists administered peripherally increase colonic propulsive motility and fecal output in experimental animals. In addition, endogenous CRF‐related peptides are found in the lower gastrointestinal (GI) tissues, suggesting a local expression of CRF receptors. In the present study, we report the expression of both CRF receptor type 1 (CRF1) and 2 (CRF2) in the rat colon at the mRNA and protein levels. For the purpose of receptor protein mapping, a specific antiserum against the C‐terminus of CRF2(2064a‐CRF2) was generated and characterized. This antiserum in conjunction with a selective anti‐CRF1antiserum (4467a‐CRF1) was used in immunofluorescent staining to demonstrate the anatomical distribution of receptor protein expression. Using RT‐PCR for the CRF1and CRF2genes, both receptor gene transcripts were found in RNA isolated from crude colonic samples. CRF1was found in the goblet and stem cells of the colonic crypts and in scattered cells of the surface epithelium and the lamina propria of the proximal colonic mucosa. In addition, double staining against neuron‐specific antigens revealed CRF1expression in the myenteric and submucosal nervous plexus. CRF2expression was localized mainly in the luminal surface of the crypts and in blood vessels of the submucosal layer. These results demonstrate expression of both CRF receptor types in the rat colon and support a role for their involvement in regulating peripheral effects of CRF ligands.
Spinophilin is phosphorylated by Ca2+/calmodulin‐dependent protein kinase II resulting in regulation of its binding to F‐actin
Authors: Grossman Stacie D. , Futter Marie , Snyder Gretchen L. , Allen Patrick B. , Nairn Angus C. , Greengard Paul , Hsieh‐Wilson Linda C. 
Published: July 2004

AbstractSpinophilin is a protein phosphatase‐1‐ and actin‐binding protein that modulates excitatory synaptic transmission and dendritic spine morphology. We have recently shown that the interaction of spinophilin with the actin cytoskeleton depends upon phosphorylation by protein kinase A. We have now found that spinophilin is phosphorylated by Ca2+/calmodulin‐dependent protein kinase II (CaMKII) in neurons. Ca2+/calmodulin‐dependent protein kinase II, located within the post‐synaptic density of dendritic spines, is known to play a role in synaptic plasticity and is ideally positioned to regulate spinophilin. Using tryptic phosphopeptide mapping, site‐directed mutagenesis and microsequencing analysis, we identified two sites of CaMKII phosphorylation (Ser‐100 and Ser‐116) within the actin‐binding domain of spinophilin. Phosphorylation by CaMKII reduced the affinity of spinophilin for F‐actin. In neurons, phosphorylation at Ser‐100 by CaMKII was Ca2+ dependent and was associated with an enrichment of spinophilin in the synaptic plasma membrane fraction. These results indicate that spinophilin is phosphorylated by multiple kinases in vivo and that differential phosphorylation may target spinophilin to specific locations within dendritic spines.
Somatic and axonal effects of ATP via P2X2 but not P2X7 receptors in rat thoracolumbar sympathetic neurones
Authors: Allgaier C. , Reinhardt R. , Schädlich H. , Rubini P. , Bauer S. , Reichenbach A. , Illes P. 
Published: July 2004

AbstractExcitatory ATP responses in rat cultured thoracolumbar sympathetic neurones are mediated by somatic P2X2 receptors. The present study investigated a possible role of axonal P2X2 as well as P2X7 receptors on the same preparation. Confocal laser scanning microscopy demonstrated P2X2 and P2X7 immunoreactivity along the axons as well as P2X7 immunoreactivity surrounding the cell nuclei. P2X7 mRNA expression was detected in individual neurones using a single‐cell RT–PCR approach. Adenosine triphosphate (ATP) caused a significant increase in axonal Ca2+ concentration which was dependent on external Ca2+ but insensitive to depletion of the cellular Ca2+ pools by cyclopiazonic acid. Pyridoxal‐phosphate‐6‐azophenyl‐2′,4′‐disulfonate (PPADS; 30 µm) virtually abolished the ATP response, whereas brilliant blue G (0.1 µm), a selective P2X7 receptor antagonist, had no effect. Dibenzoyl‐ATP (BzATP; 100 µm) induced a much smaller increase in axonal [Ca2+] concentration than ATP at equimolar concentrations. The response to BzATP was distinctly reduced by PPADS but not by brilliant blue G. The overall pharmacological profile of the axonal P2X receptors resembled closely that of the somatic P2X2 receptors. In conclusion, the present data suggest the occurrence of axonal excitatory P2X2 receptors in thoracolumbar sympathetic neurones. However, the functional significance of axonal and (peri)‐nuclear P2X7 receptors has still to be proven.
Novel isoforms of tau that lack the microtubule‐binding domain
Authors: Luo Min‐hua , Tse Sze‐Wah , Memmott John , Andreadis Athena 
Published: July 2004

AbstractTau is a microtubule‐associated protein (MAP) whose transcript undergoes complex regulated splicing in the mammalian nervous system. Our previous work with exon 6 established that tau shows a unique expression pattern and splicing regulation profile, and that it utilizes alternative splice sites in several human tissues. The mRNAs from these splicing events, if translated, would result in truncated tau variants that lack the microtubule‐binding domain. In this study, we demonstrate that at least one of these tau variants is present as a stable protein in several tissues. The novel isoform shows a localization distinct from that of canonical tau in SH‐SY5Y neuroblastoma cells which stably overexpress it. In both normal and Alzheimer's hippocampus, the novel isoform is found in dentate gyrus granular cells and CA1/CA3 pyramidal cells. However, it does not co‐localize with canonical tau but, rather, partly co‐localizes with MAP2.
Annular α‐synuclein species from purified multiple system atrophy inclusions
Authors: Pountney Dean L. , Lowe Rachel , Quilty Marian , Vickers James C. , Voelcker Nicolas H. , Gai Wei Ping 
Published: July 2004

AbstractOligodendroglial cytoplasmic inclusions composed of α‐synuclein filamentous aggregates are the pathological hallmark of multiple system atrophy (MSA). We found that cortical tissue from MSA cases contains increased detergent‐resistant high‐molecular‐weight α‐synuclein species. To analyse these species, we immunopurified α‐synuclein aggregates from pathological samples and examined their ultrastructures using scanning electron and atomic force microscopies. Purified aggregates consisted of bundles of filaments. After treatment with 1% sarcosine or 2% 3‐[(3‐cholamidopropyl) dimethyl‐ammonio]‐1‐propanesulfonate (CHAPS) detergents, we observed frequent 30–50 nm annular particles, probably released from pathological aggregates due to the dissociation of filaments by the detergents. Antibody recognition imaging using a specific anti‐α‐synuclein antibody confirmed that the annular structures were positive for α‐synuclein. In contrast to pathological α‐synuclein, detergent treatment of recombinant α‐synuclein yielded only smaller, 10–18 nm spherical particles. Our results demonstrate that detergent treatment of pathological MSA α‐synuclein aggregates, but not recombinant α‐synuclein, yields discrete α‐synuclein‐positive species with annular morphologies. The ability of the pathological α‐synuclein to form annular aggregates may be an important factor contributing to the toxicity of the protein in disease that may have implications in designing therapeutic strategies aimed at detoxifying α‐synuclein aggregates.
Methane production by microbial mats under low sulphate concentrations
Authors: BEBOUT BRAD M. , HOEHLER TORI M. , THAMDRUP BO , ALBERT DAN , CARPENTER STEVEN P. , HOGAN MARY , TURK KENDRA , DES MARAIS DAVID J. 
Published: July 2004

ABSTRACTCyanobacterial mats collected in hypersaline salterns were incubated in a greenhouse under low sulphate concentrations ([]) and examined for their primary productivity and emissions of methane and other major carbon species. Atmospheric greenhouse warming by gases such as carbon dioxide and methane must have been greater during the Archean than today in order to account for a record of moderate to warm palaeoclimates, despite a less luminous early sun. It has been suggested that decreased levels of oxygen and sulphate in Archean oceans could have significantly stimulated microbial methanogenesis relative to present marine rates, with a resultant increase in the relative importance of methane in maintaining the early greenhouse. We maintained modern microbial mats, models of ancient coastal marine communities, in artificial brine mixtures containing both modern [] (c. 70 mm) and ‘Archean’[] (<0.2 mm). At low [], primary production in the mats was essentially unaffected, while rates of sulphate reduction decreased by a factor of three, and methane fluxes increased by up to 10‐fold. However, remineralization by methanogenesis still amounted to less than 0.4% of the total carbon released by the mats. The relatively low efficiency of conversion of photosynthate to methane is suggested to reflect the particular geometry and chemical microenvironment of hypersaline cyanobacterial mats. Therefore, such mats were probably relatively weak net sources of methane throughout their 3.5 Ga history, even during periods of low environmental levels oxygen and sulphate.