bluuebunny/crossref_metadata_2025_split huggingface dataset:
The arbuscular mycorrhizal fungi of Hyacinthoides non‐scripta II. Seasonal and spatial patterns of fungal populations
Authors: MERRYWEATHER JAMES , FITTER ALASTAIR 
Published: March 2003

Roots of bluebell (Hyacinthoides non‐scripta (L.) Chouard ex Rothm.) are colonized by a range of fungal symbionts from several genera of the order Glomales. Using the identification scheme described in Merryweather & Fitter (1998), arbuscular mycorrhizal (AM) fungi in bluebell roots were quantified throughout the single growing season of 1994–5 and compared with populations of spores found in the soil around the roots.In the early part of the growing season, when its activity is entirely subterranean (autumn and winter), bluebell habitually associates with a Scutellospora morphotype which is almost certainly S. dipurpurescens Morton & Koske (emend. Walker, 1993) whose spores occur in the root zone. This is the time of maximum phosphorus inflow and bulb‐stored carbohydrate utilization by this mycorrhiza. A diverse flora of other AM fungal morphotypes (Acaulospora and Glomus), which might also form mycorrhizas with other plants in the vicinity of bluebells, invade the roots later in the season (spring), when P inflow is reduced and carbohydrate is available as fresh photosynthate. Their contribution to the mycorrhiza might be less than that of Scutellospora, particularly in terms of P assimilation.Both AM fungi in roots and glomalean spores recovered from soil around bluebell roots showed a significant degree of correlation with the vegetation within which the test plants grew. In the case of AM fungi in roots, Scutellospora showed no special preference for either, but Glomus correlated with a canopy of sycamore (Acer pseudoplatanus L.) and Acaulospora with oak (Quercus petraea (Mattuschka) Liebl.). Spores which most closely resembled S. dipurpurescens and Acaulospora gerdemannii Schenck & Nicolson were significantly more numerous under sycamore, but a spore like Acaulospora koskei Blaskowski, the most numerous and frequently encountered glomalean spore in the system, showed no preference for areas dominated by either tree. There was no significant relationship between AM fungal populations in bluebell roots and glomalean spores recovered from associated soil.The two spore taxa most frequently found in the vicinity of bluebell roots (A. koskei and S. dipurpurescens) were also found in lower numbers in soil from a region of the field site in which bluebell was absent, indicating that the main bluebell AM fungi do not exclusively associate with that host.
Uptake of glycine by field grown wheat
Authors: Näsholm Torgny , Huss‐Danell Kerstin , Högberg Peter 
Published: March 2003

Summary

Uptake of glycine, a simple organic nitrogen (N) source, directly from the soil is shown here in a conventionally cropped wheat ( Triticum aestivum ) field.
Wheat plants were harvested after tracer injections into the soil of two forms of dual‐labelled amino acid; [ 13C2], [15N]‐glycine and 2‐[13C], [15N]‐glycine. Uptake of intact amino acid was analysed by stable isotope–, and gas chromatography–, mass spectrometry.
Significant increases in 13
C were found in root extracts for all glycine‐treated plants. Regression analysis of excess
13
C vs excess
15 N for the two glycine forms showed that at least 20% of absorbed glycine‐N was derived from uptake of intact glycine. Gas chromatography–mass spectrometry was used to verify the presence of intact dual‐labelled glycine in wheat roots. Results also indicated that glycine decarboxylase had a minor role in metabolism of absorbed glycine in wheat roots. Microbial metabolism in the soil did, however, result in rapid decarboxylation of added glycine.
Field‐grown wheat takes up glycine directly from the soil; the dependence of agricultural plants on nitrate and ammonium as the only forms of available N is therefore questionable.
Seedling performance of pasture species under elevated CO2
Authors: Edwards G. R. , Newton P. C. D. , Tilbrook J. C. , Clark H. 
Published: March 2003

Summary

The effects of elevated CO2 on seedling recruitment are presented for the pasture species Anthoxanthum odoratum, Cerastium glomeratum, Leontodon saxatilis, Lolium perenne, Poa pratensis and Trifolium repens.
Seeds collected from pastures maintained at ambient (360 µl l−1) and elevated (475 µl l−1) CO2 were measured for germination and seedling growth in a reciprocal design under ambient and elevated CO2.
Seedlings of A. odoratum and L. perenne from elevated‐CO2‐developed seeds were heavier than those from ambient‐CO2‐developed seeds but only when the seedlings were grown at elevated CO2. Elevated‐CO2‐developed seeds had higher germination and seedling mass in T. repens and lower germination and seedling mass in L. saxatilis, irrespective of the CO2 concentration after sowing. There were more L. saxatilis and T. repens seedlings in pastures maintained at elevated than ambient CO2; a seed addition experiment showed that this was due mainly to the increased seed production of these species under elevated CO2. Seedling recruitment of C. glomeratum and P. pratensis was unaffected by elevated CO2.
Species exhibited variable responses to seed development under elevated CO2 that could potentially alter community composition by influencing seedling recruitment.
Emodin – a secondary metabolite with multiple ecological functions in higher plants
Authors: Izhaki Ido 
Published: March 2003

SummaryThe anthraquinone emodin, identified in 17 plant families distributed worldwide, has numerous biological activities, some of which exhibit a wide spectrum of ecological impacts by mediating biotic or abiotic interactions of plants with their environment. Here the evidence for direct and indirect effects of emodin on plant survival and reproduction is reviewed. Emodin in vegetative organs may help protect plants against herbivores, pathogens, competitors and extrinsic abiotic factors (e.g. high light intensities). In unripe fruit pulp, emodin may facilitate seed dispersal by protecting the immature fruit against predispersal seed predation whereas in ripe pulp it may deter frugivores and thus reduce the chances that seeds will be defecated beneath the parent plant. It also accelerates the passage of seeds through the digestive tract, potentially reducing dispersal distance and increasing seed viability upon dispersal. In certain circumstances both of the last two effects could also have negative fitness consequences for plants. Natural selection should favor secondary metabolites with multiple functions because they protect the plants against a variety of unpredictable biotic and abiotic environments. Such metabolites also enhance plant defenses by using different molecular targets of specific enemies through a variety of mechanisms of action. Emodin illustrates the wide and often overlooked potential for chemical multifunctionality in plant secondary metabolites.
The effects of commercial starter culture and storage temperature on the oxidative stability and diacetyl production in butter
Authors: Bakirci Ihsan , Çelik Serafettin , Özdemir Cihat 
Published: March 2003

In this study, the effects of four different direct‐vat‐set (DVS) commercial starter cultures (CHN11, CHN22, EZAL BT001 and MM100) and storage temperatures (4 ± 1 and −18 ± 2°C) on the oxidative stability and diacetyl production in butter during a 4‐month period were investigated. Samples were taken from butter on days 3, 30, 60, 90 and 120. Analyses of titration acidity, peroxide value, free fatty acids and diacetyl contents of the samples taken were carried out. The effects of the starter cultures on the peroxide value and diacetyl contents were found to be significant (P < 0.01) while the storage temperatures significantly affected all parameters tested. Interaction between the type of culture and storage temperature was significant for free fatty acids (P < 0.05) and diacetyl content (P < 0.01).
Characterization of the blood–brain barrier choline transporter using the in situ rat brain perfusion technique
Authors: Allen David D. , Smith Quentin R. 
Published: March 2003

Choline enters brain by saturable transport at the blood–brain barrier (BBB). In separate studies, both sodium‐dependent and passive choline transport systems of differing affinity have been reported at brain capillary endothelial cells. In the present study, we re‐examined brain choline uptake using the in situ rat brain perfusion technique. Saturable brain choline uptake from perfusion fluid was best described by a model with a single transporter (Vmax= 2.4–3.1 nmol/min/g; Km = 39–42 µm) with an apparent affinity (1/Km) for choline five to ten‐fold greater than previously reported in vivo, but less than neuronal ‘high‐affinity’ brain choline transport (Km = 1–5 µm). BBB choline uptake from a sodium‐free perfusion fluid using sucrose for osmotic balance was 50% greater than in the presence of sodium suggesting that sodium is not required for transport. Hemicholinium‐3 inhibited brain choline uptake with a Ki (57 ± 11 µm) greater than that at the neuronal choline system. In summary, BBB choline transport occurs with greater affinity than previously reported, but does not match the properties of the neuronal choline transporter. The Vmax of this system is appreciable and may provide a mechanism for delivering cationic drugs to brain.
Neurotoxic Aβ peptides increase oxidative stress in vivo through NMDA‐receptor and nitric‐oxide‐synthase mechanisms, and inhibit complex IV activity and induce a mitochondrial permeability transition in vitro
Authors: Parks Janice K. , Smith Trisha S. , Trimmer Patricia A. , Bennett James P. , Parker W. Davis 
Published: March 2003

Beta amyloid (Aβ) peptides accumulate in Alzheimer's disease and are neurotoxic possibly through the production of oxygen free radicals. Using brain microdialysis we characterized the ability of Aβ to increase oxygen radical production in vivo. The 1–40 Aβ fragment increased 2,3‐dehydroxybenzoic acid efflux more than the 1–28 fragment, in a manner dependent on nitric oxide synthase and NMDA receptor channels. We then examined the effects of Aβ peptides on mitochondrial function in vitro. Induction of the mitochondrial permeability transition in isolated rat liver mitochondria by Aβ(25–35) and Aβ(35–25) exhibited dose dependency and required calcium and phosphate. Cyclosporin A prevented the transition as did ruthenium red, chlorpromazine, or N‐ethylmaleimide. ADP and magnesium delayed the onset of mitochondrial permeability transition. Electron microscopy confirmed the presence of Aβ aggregates and swollen mitochondria and preservation of mitochondrial structure by inhibitors of mitochondrial permeability transition. Cytochrome c oxidase (COX) activity was selectively inhibited by Aβ(25–35) but not by Aβ(35–25). Neurotoxic Aβ peptide can increase oxidative stress in vivo through mechanisms involving NMDA receptors and nitric oxide sythase. Increased intracellular Aβ levels can further exacerbate the genetically driven complex IV defect in sporadic Alzheimer's disease and may precipitate mitochondrial permeability transition opening. In combination, our results provide potential mechanisms to support the feed‐forward hypothesis of Aβ neurotoxicity.
Pitx3 activates mouse tyrosine hydroxylase promoter via a high‐affinity binding site
Authors: Lebel Mélanie , Gauthier Yves , Moreau Alain , Drouin Jacques 
Published: March 2003

Tyrosine hydroxylase (TH) is the rate‐limiting enzyme of dopamine and (nor)adrenaline biosynthesis. Regulation of its gene expression is complex and different regulatory mechanisms appear to be operative in various neuronal lineages. Pitx3, a homeodomain‐containing transcription factor, has been cloned from neuronal tissues and, in the CNS, mouse Pitx3 is exclusively expressed in midbrain dopaminergic (MesDA) neurons from embryonic day 11 (E11). TH appears in these neurons at E11.5, consistent with a putative role of Pitx3 in TH transcription. We show that Pitx3 activates the TH promoter through direct interaction with a single high‐affinity binding site within the promoter and that this site is sufficient for Pitx3 responsiveness. In contrast, we did not observe an effect of Nurr1, an orphan nuclear receptor essential for normal development of MesDA neurons, on TH promoter activity. Pitx3 activation of TH promoter activity appears to be cell‐dependent suggesting that Pitx3 action may be modulated by other(s) regulatory mechanism(s) and factor(s).
Nitric oxide regulates adenylyl cyclase activity in rat striatal membranes
Authors: Hudson Tracie Y. , Corbett John A. , Howlett Allyn C. , Klein Claudette 
Published: March 2003

The regulation of adenylyl cyclase activity by nitric oxide (NO) was studied in rat (Sprague–Dawley) striatal membranes. Three chemically distinct NO donors attenuated forskolin‐stimulated activity but did not alter basal activity. Maximum inhibition resulted in a 50% decrease in forskolin‐stimulated activity, consistent with the presence of multiple isoforms of adenylyl cyclase and our previous findings that only the forskolin‐stimulated activity of the type‐5 and ‐6 isoform family of enzymes is inhibited by NO. To monitor primarily the type‐5 isoform, we examined the ability of NO donors to attenuate D1‐agonist‐stimulated adenylyl cyclase activity. Under those conditions, complete inhibition was observed. The data indicate that NO attenuates neuromodulator‐stimulated cAMP signaling in the striatum.
Mimicking the nicotinic receptor binding site by a single chain Fv selected by competitive panning from a synthetic phage library
Authors: Bracci Luisa , Pini Alessandro , Lozzi Luisa , Lelli Barbara , Battestin Paola , Spreafico Adriano , Bernini Andrea , Niccolai Neri , Neri Paolo 
Published: March 2003

We have developed a novel competitive method to select from a phage display library a single chain Fv which is able to mimic the α‐bungarotoxin binding site of the muscle nicotinic receptor. The single chain Fv was selected from a large synthetic library using α‐bungarotoxin‐coated magnetic beads. Toxin‐bound phages were then eluted by competition with affinity purified nicotinic receptor. Recognition of the toxin by the anti‐α‐bungarotoxin single chain Fv was very similar to that of the receptor, such as indicated by the epitope mapping of α‐bungarotoxin through overlapping synthetic peptides. Moreover, several positively charged residues located in the toxin second loop and in the C‐terminal region were found to be critical, to a similar extent, for toxin recognition by the single chain Fv and the receptor. However, although the anti‐α‐bungarotoxin single chain Fv seems to mimic the toxin binding site of the nicotinic receptor, it does not bind other nicotinic agonists or antagonists. Our results suggest that competitive selection of anti‐ligand antibody phages can allow the production of receptor‐mimicking molecules directly and exclusively targeted at one specific ligand. Since physiologically and pharmacologically different ligands can produce opposite effects on receptor functions, such selective ligand decoys can have important therapeutic applications.
The chemokine interleukin‐8 acutely reduces Ca2+ currents in identified cholinergic septal neurons expressing CXCR1 and CXCR2 receptor mRNAs
Authors: Puma Carole , Danik Marc , Quirion Rémi , Ramon Fabienne , Williams Sylvain 
Published: March 2003

The chemokine IL‐8 is known to be synthesized by glial cells in the brain. It has traditionally been shown to have an important role in neuroinflammation but recent evidence indicates that it may also be involved in rapid signaling in neurons. We investigated how IL‐8 participates in rapid neuronal signaling by using a combination of whole‐cell recording and single‐cell RT‐PCR on dissociated rat septal neurons. We show that IL‐8 can acutely reduce Ca2+ currents in septal neurons, an effect that was concentration‐dependent, involved the closure of L‐ and N‐type Ca2+ channels, and the activation of Giα1 and/or Giα2 subtype(s) of G‐proteins. Analysis of the mRNAs from the recorded neurons revealed that the latter were all cholinergic in nature. Moreover, we found that all cholinergic neurons that responded to IL‐8, expressed mRNAs for either one or both IL‐8 receptors CXCR1 and CXCR2. This is the first report of a chemokine that modulates ion channels in neurons via G‐proteins, and the first demonstration that mRNAs for CXCR1 are expressed in the brain. Our results suggest that IL‐8 release by glial cells in vivo may activate CXCR1 and CXCR2 receptors on cholinergic septal neurons and acutely modulate their excitability by closing calcium channels.
Multiple pathways of Pb2+ permeation in rat cerebellar granule neurones
Authors: Mazzolini Monica , Traverso Sonia , Marchetti Carla 
Published: March 2003

The pathways of lead (Pb2+) uptake were studied in fura‐2‐loaded cerebellar granule cells from 8‐day‐old rats. In a nominal Ca‐free external bath, Pb2+ (5–50 µm) determined an increase of the fluorescence emission ratio (R = E340/E380) even in the absence of any specific stimulus. This rise was dose‐dependent, was not significantly affected by mm Mg2+ or Ca2+, but it was readily reversed by the membrane‐permeant heavy metal chelator tetrakis(2‐pyridylmethyl) ethylene‐diamine (TPEN, 100 µm), indicating that it was due to Pb2+ influx. The rate of rise, dR/dt, was increased up to a factor of 5 by depolarizing high‐KCl solution, indicating a sizeable permeation through voltage‐dependent channels. This effect was neither antagonized by nimodipine, nor enhanced by BayK8644, but it was slackened by ω‐agatoxin IVA (200 nm), suggesting an involvement of non‐L‐type calcium channels. Pb2+ influx was also stimulated by glutamic acid or NMDA in the presence of 10–30 µm glycine, but only in Mg‐free solution, suggesting that glutamate channels of the NMDA type are an additional pathway of Pb2+ uptake. Pb2+ caused a time‐, dose‐ and stimulus‐dependent saturation of the dye, whose intracellular concentration is ∼ 10 µm, indicating that intracellular Pb2+ can readily reach a concentration in the micromolar range. These results indicate that the particular vulnerability of neurones to Pb2+ poisoning is linked to the presence of specific transport systems, which mediate the rapid uptake of Pb2+ into the neurone.
Modulation of intracellular calcium changes and glutamate release by neuropeptide Y1 and Y2 receptors in the rat hippocampus: differential effects in CA1, CA3 and dentate gyrus
Authors: Silva Ana P. , Carvalho Arsélio P. , Carvalho Caetana M. , Malva João O. 
Published: March 2003

In the present work, we investigated the role of pre‐ and post‐synaptic neuropeptide Y1 (NPY1) and Y2 receptors on the calcium responses and on glutamate release in the rat hippocampus. In cultured hippocampal neurones, we observed that only NPY1 receptors are involved in the modulation of intracellular free calcium concentration ([Ca2+]i). In 88% of the neurones analysed, the increase in the [Ca2+]i, in response to depolarization with 50 mm KCl, was inhibited by 1 µm[Leu31,Pro34]NPY, whereas 300 nm NPY13–36 was without effect. However, studies with hippocampal synaptosomes showed that both NPY1 and Y2 receptors can modulate the [Ca2+]i and glutamate release. The pharmacological characterization of the NPY‐induced inhibition of glutamate release indicated that Y2 receptors play a predominant role, both in the modulation of Ca2+‐dependent and ‐independent glutamate release. However, we could distinguish between Y1 and Y2 receptors by using [Leu31,Pro34]NPY and NPY13–36. Active pre‐synaptic Y1 receptors are present in the dentate gyrus (DG) as well as in the CA3 subregion, but its activity was not revealed by using the endogenous agonist, NPY. Concerning the Y2 receptors, they are present in the three subregions (CA1, CA3 and DG) and were activated by either NPY13–36 or NPY. The present data support a predominant role for NPY2 receptors in mediating NPY‐induced inhibition of glutamate release in the hippocampus, but the physiological relevance of the presently described DG and CA3 pre‐synaptic NPY1 receptors remains to be clarified.
Nicotine‐induced phosphorylation of extracellular signal‐regulated protein kinase and CREB in PC12h cells
Authors: Nakayama Hitoshi , Numakawa Tadahiro , Ikeuchi Toshihiko , Hatanaka Hiroshi 
Published: March 2003

We have investigated mechanisms of nicotine‐induced phosphorylation of extracellular signal‐regulated protein kinase (p42/44 MAP kinase, ERK) and cAMP response element binding protein (CREB) in PC12h cells. Nicotine transiently induced ERK phosphorylation at more than 1 µm. The maximal level of nicotine‐induced ERK phosphorylation was lower than that of the membrane depolarization induced and, to a great extent, the nerve growth factor (NGF)‐induced ERK phosphorylation. Nicotinic acetylcholine receptor (nAChR) α7 subunit‐selective inhibitors had no significant effect on nicotine‐induced ERK phosphorylation. l‐Type voltage‐sensitive calcium channel antagonists inhibited nicotine‐induced ERK phosphorylation. Calcium imaging experiments showed that α7‐containing nAChR subtypes were functional at 1 µm of nicotine in the nicotine‐induced calcium influx, and non‐α7 nAChRs were prominent in the Ca2+ influx at 50 µm of nicotine. An expression of dominant inhibitory Ras inhibited nicotine‐induced ERK phosphorylation. A calmodulin antagonist, a CaM kinase inhibitor, a MAP kinase kinase inhibitor inhibited nicotine‐induced ERK and CREB phosphorylation. The time course of the phosphorylation of CREB induced by nicotine was similar to that of ERK induced by nicotine. These results suggest that non‐α7 nAChRs are involved in nicotine‐induced ERK phosphorylation through CaM kinase and the Ras‐MAP kinase cascade and most of the nicotine‐induced CREB phosphorylation is mediated by the ERK phosphorylation in PC12h cells.
Integrative nuclear FGFR1 signaling (INFS) pathway mediates activation of the tyrosine hydroxylase gene by angiotensin II, depolarization and protein kinase C
Authors: Peng, Hu , Myers, Jason , Fang, Xiaohong , Stachowiak,* Ewa K. , Maher, Pamela A. , Martins, Gabriel G. , Popescu Gabriela , Berezney‡ Ronald , Stachowiak Michal K. 
Published: March 2003

AbstractThe integrative nuclear FGFR1 signaling (INFS) pathway functions in association with cellular growth, differentiation, and regulation of gene expression, and is activated by diverse extracellular signals. Here we show that stimulation of angiotensin II (AII) receptors, depolarization, or activation protein kinase C (PKC) or adenylate cyclase all lead to nuclear accumulation of fibroblast growth factor 2 (FGF‐2) and FGFR1, association of FGFR1 with splicing factor‐rich domains, and activation of the tyrosine hydroxylase (TH) gene promoter in bovine adrenal medullary cells (BAMC). The up‐regulation of endogenous TH protein or a transfected TH promoter‐luciferase construct by AII, veratridine, or PMA (but not by forskolin) is abolished by transfection with a dominant negative FGFR1TK‐mutant which localizes to the nucleus and plasma membrane, but not by extracellularly acting FGFR1 antagonists suramin and inositolhexakisphosphate (IP6). Mechanism of TH gene activation by FGF‐2 and FGFR1 was further investigated in BAMC and human TE671 cultures. TH promoter was activated by co‐transfected HMW FGF‐2 (which is exclusively nuclear) but not by cytoplasmic FGF‐1 or extracellular FGFs. Promoter transactivation by HMWFGF‐2 was accompanied by an up‐regulation of FGFR1 specifically in the cell nucleus and was prevented FGFR1(TK‐) but not by IP6 or suramin. The TH promoter was also transactivated by co‐transfected wild‐type FGFR1, which localizes to both to the nucleus and the plasma membrane, and by an exclusively nuclear, soluble FGFR1(SP‐/NLS) mutant with an inserted nuclear localization signal. Activation of the TH promoter by nuclear FGFR1 and FGF‐2 was mediated through the cAMP‐responsive element (CRE) and was associated with induction of CREB‐ and CBP/P‐300‐containing CRE complexes. We propose a new model for gene regulation in which nuclear FGFR1 acts as a mediator of CRE transactivation by AII, cell depolarization, and PKC.