bluuebunny/crossref_metadata_2025_split huggingface dataset:
Niche properties and geographical extent as predictors of species sensitivity to climate change
Authors: Thuiller Wilfried , Lavorel Sandra , Araújo Miguel B. 
Published: June 2005

ABSTRACTAim  Bioclimatic envelope models are often used to make projections of species’ potential responses to climate change. It can be hypothesized that species with different kinds of distributions in environmental niche and geographical space may respond differently to changes in climate. Here, we compare projections of shifts in species ranges with simple descriptors of species niche (position and breadth) and geographical (range size) distributions.Location  Europe.Methods  The future distribution for 1200 European plant species were predicted by niche‐based models using seven climate variables known to have an important role in limiting plant species distributions. Ecological niche properties were estimated using a multivariate analysis. Species range changes were then related to species niche properties using generalized linear models.Results  Generally, percentage of remaining suitable habitat in the future increased linearly with niche position and breadth. Increases in potential suitable habitat were associated with greater range size, and had a hump‐shaped relationship with niche position on temperature gradient. By relating species chorotypes to percentage of remaining or gained habitat, we highlighted biogeographical patterns of species sensitivity to climate change. These were clearly related to the degree of exposure according to regional patterns of projected climate change.Main conclusion  This study highlights general patterns about the relationships between sensitivity of species to climate change and their ecological properties. There is a strong convergence between simple inferences based on ecological characteristics of species and projections by bioclimatic ‘envelope’ models, confirming macroecological assumptions about species sensitivity based on niche properties. These patterns appear to be most strongly driven by the exposure of species to climate change, with additional effects of species niche characteristics. We conclude that simple species niche properties are powerful indicators of species’ sensitivity to climate change.
The interspecific range size–body size relationship in Australian frogs
Authors: Murray Brad R. , Hose Grant C. 
Published: June 2005

ABSTRACTAim There is substantial residual scatter about the positive range size–body size relationship in Australian frogs. We test whether species’ life history and abundance can account for this residual scatter.Location Australia.Methods Multiple regressions were performed using both cross‐species and independent contrasts analyses to determine whether clutch size, egg size and species abundance account for variation in range size over and above the effects of body size.Results In both cross‐species and independents contrasts models with body size, clutch size and egg size as predictors, partialr2values revealed that only egg size was significantly and uniquely related to range size. Contrary to expectation, neither body size nor clutch size could account for significant variation in range size. Incorporating species abundance as a predictor in further multiple regression analysis demonstrated that while abundance accounted for a significant proportion of range size variation, the contribution of egg size was reduced but still significant. Notably, non‐significant relationships persisted between range size and both body size and clutch size.Conclusions The weak positive correlation between body size and range size in Australian frogs disappears after accounting for species abundance and egg size. Our findings demonstrate that species with both high local abundance and small eggs occupy comparatively wider geographical ranges than species with low abundance and large eggs.
Amyloid beta peptide 1–40 enhances the action of Toll‐like receptor‐2 and ‐4 agonists but antagonizes Toll‐like receptor‐9‐induced inflammation in primary mouse microglial cell cultures
Authors: Lotz Miriam , Ebert Sandra , Esselmann Hermann , Iliev Asparouh I. , Prinz Marco , Wiazewicz Nicole , Wiltfang Jens , Gerber Joachim , Nau Roland 
Published: June 2005

AbstractThe interaction of endogenous and exogenous stimulators of innate immunity was examined in primary cultures of mouse microglial cells and macrophages after application of defined Toll‐like receptor (TLR) agonists [lipopolysaccharide (LPS) (TLR4), the synthetic lipopeptide Pam3Cys‐Ser‐Lys4 (Pam3Cys) (TLR2) and single‐stranded unmethylated CpG‐DNA (CpG) (TLR9)] alone and in combination with amyloid beta peptide (Abeta) 1–40. Abeta 1–40 stimulated microglial cells and macrophages primed by interferon‐γ in a dose‐dependent manner. Co‐administration of Abeta1–40 with LPS or Pam3Cys led to an additive release of nitric oxide (NO) and tumour necrosis factor alpha (TNF‐α). This may be one reason for the clinical deterioration frequently observed in patients with Alzheimer's disease during infections. In contrast, co‐application of Abeta1–40 with CpG led to a substantial decrease of NO and TNF‐ α release compared with stimulation with CpG alone. Abeta 1–40 and CpG did not co‐localize within the same subcellular compartment, making a direct physicochemical interaction as the cause of the observed antagonism very unlikely. This suggests that not all TLR agonists enhance the stimulatory effect of Abeta on innate immunity.
NADPH oxidase is required for NMDA receptor‐dependent activation of ERK in hippocampal area CA1
Authors: Kishida Kenneth T. , Pao Maryland , Holland Steven M. , Klann Eric 
Published: June 2005

AbstractPrevious studies have shown that N‐methyl‐d‐aspartate (NMDA) receptor activation results in production of reactive oxygen species (ROS) and activation of extracellular signal‐regulated kinase (ERK) in hippocampal area CA1. In addition, application of ROS to hippocampal slices has been shown to result in activation of ERK in area CA1. To determine whether these events were linked causally, we investigated whether ROS are required for NMDA receptor‐dependent activation of ERK. In agreement with previous studies, we found that treatment of hippocampal slices with NMDA resulted in activation of ERK in area CA1. The NMDA receptor‐dependent activation of ERK was either blocked or attenuated by a number of antioxidants, including the general antioxidant N‐acetyl‐l‐cysteine (L‐NAC), the superoxide‐scavenging enzyme superoxide dismutase (SOD), the membrane‐permeable SOD mimetic Mn(III) tetrakis (4‐benzoic acid) porphyrin (MnTBAP), the hydrogen peroxide‐scavenging enzyme catalase, and the catalase mimetic ebselen. The NMDA receptor‐dependent activation of ERK also was blocked by the NADPH oxidase inhibitor diphenylene iodonium (DPI) and was absent in mice that lacked p47phox, one of the required protein components of NADPH oxidase. Taken together, our results suggest that ROS production, especially superoxide production via NADPH oxidase, is required for NMDA receptor‐dependent activation of ERK in hippocampal area CA1.
Histone methylation at gene promoters is associated with developmental regulation and region‐specific expression of ionotropic and metabotropic glutamate receptors in human brain
Authors: Stadler Florian , Kolb Gabriele , Rubusch Lothar , Baker Stephen P. , Jones Edward G. , Akbarian Schahram 
Published: June 2005

AbstractGlutamatergic signaling is regulated, in part, through differential expression of NMDA and AMPA/KA channel subunits and G protein‐coupled metabotropic receptors. In human brain, region‐specific expression patterns of glutamate receptor genes are maintained over the course of decades, suggesting a role for molecular mechanisms involved in long‐term regulation of transcription, including methylation of lysine residues at histone N‐terminal tails. Using a native chromatin immunoprecipitation assay, we studied histone methylation marks at proximal promoters of 16 ionotropic and metabotropic glutamate receptor genes (GRIN1,2A–D; GRIA1,3,4; GRIK2,4,5; GRM1,3,4,6,7 ) in cerebellar cortex collected across a wide age range from midgestation to 90 years old. Levels of di‐ and trimethylated histone H3‐lysine 4, which are associated with open chromatin and transcription, showed significant differences between promoters and a robust correlation with corresponding mRNA levels in immature and mature cerebellar cortex. In contrast, levels of trimethylated H3‐lysine 27 and H4‐lysine 20, two histone modifications defining silenced or condensed chromatin, did not correlate with transcription but were up‐regulated overall in adult cerebellum. Furthermore, differential gene expression patterns in prefrontal and cerebellar cortex were reflected by similar differences in H3‐lysine 4 methylation at promoters. Together, these findings suggest that histone lysine methylation at gene promoters is involved in developmental regulation and maintenance of region‐specific expression patterns of ionotropic and metabotropic glutamate receptors. The association of a specific epigenetic mark, H3‐(methyl)‐lysine 4, with the molecular architecture of glutamatergic signaling in human brain has potential implications for schizophrenia and other disorders with altered glutamate receptor function.
Cellular localization and subcellular distribution of Unc‐33‐like protein 6, a brain‐specific protein of the collapsin response mediator protein family that interacts with the neuronal glycine transporter 2
Authors: Horiuchi Masahisa , Loebrich Sven , Brandstaetter Johann Helmut , Kneussel Matthias , Betz Heinrich 
Published: June 2005

AbstractUnc‐33‐like protein (Ulip)6, a brain‐specific phosphoprotein of the Ulip/collapsin response mediator protein family, was originally identified in our laboratory by yeast two‐hybrid screening using the cytoplasmic N‐terminal domain of the neuronal glycine transporter, glycine transporter (GlyT) 2, as a bait. Here, the interaction of Ulip6 with the N‐terminal domain of GlyT2 was found to be specific for this member of the Ulip/collapsin response mediator protein family and to involve amino acids 135–184 of GlyT2. In pull‐down assays and coimmunoprecipitation experiments with rat spinal cord extract, the presence of phosphatase inhibitors significantly enhanced binding of Ulip6 to GlyT2. Subcellular fractionation of spinal cord and retina homogenates at different developmental stages showed Ulip6 immunoreactivity to be associated with light vesicles that were distinct from GlyT2‐containing and synaptic vesicles. Immunocytochemistry revealed punctate Ulip6 immunoreactivity in both somatic regions and processes of cultured spinal neurones; no colocalization with GlyT2 or other synaptic marker proteins was found. In retina, which expresses only GlyT1 but not GlyT2, Ulip6 was detected in the inner plexiform layer and along the somata and processes of selected bipolar, amacrine and ganglion cells. Our data support a model in which Ulip6 transiently interacts with GlyT2 in a phosphorylation‐dependent manner.
AMPA receptor stimulation increases α5β1 integrin surface expression, adhesive function and signaling
Authors: Lin Ching‐Yi , Lynch Gary , Gall Christine M. 
Published: June 2005

AbstractIntegrin proteins are critical for stabilization of hippocampal long‐term potentiation but the mechanisms by which integrin activities are involved in synaptic transmission are not known. The present study tested whether activation of α‐amino‐3‐hydroxy‐5‐methylisoxazole‐4‐proprionate (AMPA) class glutamate receptors increases surface expression of α5β1 integrin implicated in synaptic potentiation. Surface protein biotinylation assays demonstrated that AMPA treatment of COS7 cells expressing GluR1 homomeric AMPA receptors increased membrane insertion and steady‐state surface levels of α5 and β1 subunits. Treated cells exhibited increased adhesion to fibronectin‐ and anti‐α5‐coated substrates and tyrosine kinase signaling elicited by fibronectin‐substrate adhesion, as expected if new surface receptors are functional. Increased surface expression did not occur in calcium‐free medium and was blocked by the protein kinase C inhibitor chelerythrine chloride and the exocytosis inhibitor brefeldin A. AMPA treatment similarly increased α5 and β1 surface expression in dissociated neurons and cultured hippocampal slices. In both neuronal preparations AMPA‐induced integrin trafficking was blocked by combined antagonism of NMDA receptor and L‐type voltage‐sensitive calcium channel activities but was not induced by NMDA treatment alone. These results provide the first evidence that glutamate receptor activation increases integrin surface expression and function, and suggest a novel mechanism by which synaptic activity can engage a volley of new integrin signaling in coordination with, and probably involved in, stabilization of synaptic potentiation.
Retrovirally transduced NCAM140 facilitates neuronal fate choice of hippocampal progenitor cells
Authors: Kim Ju Hee , Lee Jung‐Ha , Park Jin‐Yong , Park Chang‐Hwan , Yun Chae‐Ok , Lee Sang‐Hun , Lee Yong‐Sung , Son Hyeon 
Published: June 2005

AbstractNeural cell adhesion molecule (NCAM) influences proliferation and differentiation of neuronal cells. However, only a little is known about the downstream effects of NCAM signalling, such as alterations in gene transcription, which are associated with cell fate choice. To examine whether NCAM plays a role in cell fate choice during hippocampal neurogenesis, we performed a gain‐of‐function study, using a retroviral vector which contained full‐length NCAM140 cDNA and the marker gene EGFP, and found that NCAM140 promoted neurogenesis by activating proneural transcription activators with concurrent inhibition of gliogenesis. The enhanced transcript levels of proneural transcription factors in NCAM140‐transduced cells were down‐regulated by treatment of the cells with mitogen‐activated protein kinase kinase (MEK) inhibitor PD098059. Overall, these findings suggest that NCAM140 may facilitate hippocampal neurogenesis via regulation of proneurogenic transcription factors in an extracellular signal‐regulated kinase (ERK)‐dependent manner.
Proteomic identification of differentially expressed proteins in the aging murine olfactory system and transcriptional analysis of the associated genes
Authors: Poon H. Fai , Vaishnav Radhika A. , Butterfield D. Allan , Getchell Marilyn L. , Getchell Thomas V. 
Published: June 2005

AbstractDecline in olfactory ability has been associated with aging as well as neurodegenerative disorders. The aim of this study was to gain fundamental insight into molecular events associated with the aging olfactory system. We report a comparative proteomic analysis of the olfactory epithelium (OE) and olfactory bulb (OB) of old (80‐week old) and young (6‐week old) mice with further analysis of age‐related differences in differentially expressed proteins at the mRNA level using real‐time RT–PCR. Nine proteins in the OE and 20 in the OB were differentially expressed in old and young mice; of these, aldolase 1, peptidyl prolyl isomerase A, mitochondrial aconitase 2, mitochondrial aldehyde dehydrogenase 2 and albumin 1 were identified in the OE; and ATP synthase isoform 1, enolase 1, ferritin heavy chain, malate dehydrogenase 1, tropomyosin alpha 3 chain and dynamin 1 were identified in the OB. At the transcriptional level, aconitase 2 in the OE and ferritin heavy chain 1 in the OB were differentially expressed with aging, in concordance with the proteomic data. Our results demonstrate an altered proteomic profile of the aged murine olfactory system. The identified proteins fall into three broadly defined functional categories: (i) metabolism, (ii) transport/motility and (iii) stress response. Our transcriptional analysis provides insight into possible mechanisms by which protein expression may be regulated in the OE and OB. The results are discussed in relation to the decrement in olfactory sensitivity with aging.
Reversal of non‐hydroxy : α‐hydroxy galactosylceramide ratio and unstable myelin in transgenic mice overexpressing UDP‐galactose : ceramide galactosyltransferase
Authors: Fewou Simon N. , Büssow Heinrich , Schaeren‐Wiemers Nicole , Vanier Marie T. , Macklin Wendy B. , Gieselmann Volkmar , Eckhardt Matthias 
Published: June 2005

AbstractThe sphingolipids galactosylceramide and sulfatide are important for the formation and maintenance of myelin. Transgenic mice overexpressing the galactosylceramide synthesizing enzyme UDP‐galactose : ceramide galactosyltransferase in oligodendrocytes display an up to four‐fold increase in UDP‐galactose : ceramide galactosyltransferase activity, which correlates with an increase in its products monogalactosyl diglyceride and non‐hydroxy fatty acid‐containing galactosylceramide. Surprisingly, however, we observed a concomitant decrease in α‐hydroxylated galactosylceramide such that total galactosylceramide in transgenic mice was almost unaltered. These data suggest that UDP‐galactose : ceramide galactosyltransferase activity does not limit total galactosylceramide level. Furthermore, the predominance of α‐hydroxylated galactosylceramide appeared to be determined by the extent to which non‐hydroxylated ceramide was galactosylated rather than by the higher affinity of UDP‐galactose : ceramide galactosyltransferase for α‐hydroxy fatty acid ceramide. The protein composition of myelin was unchanged with the exception of significant up‐regulation of the myelin and lymphocyte protein. Transgenic mice were able to form myelin, which, however, was apparently unstable and uncompacted. These mice developed a progressive hindlimb paralysis and demyelination in the CNS, demonstrating that tight control of UDP‐galactose : ceramide galactosyltransferase expression is essential for myelin maintenance.
Blockade of interleukin‐6 signaling aggravates ischemic cerebral damage in mice: possible involvement of Stat3 activation in the protection of neurons
Authors: Yamashita Toru , Sawamoto Kazunobu , Suzuki Shigeaki , Suzuki Norihiro , Adachi Kazuhide , Kawase Takeshi , Mihara Masahiko , Ohsugi Yoshiyuki , Abe Koji , Okano Hideyuki 
Published: June 2005

AbstractInterleukin (IL)‐6 expression transiently increases in the acute phase of cerebral ischemia. To investigate the physiological significance of endogenous IL‐6 expression and to identify the main signal pathway for the action of IL‐6, we administered anti‐mouse IL‐6 receptor monoclonal antibody (IL‐6RA), which blocks IL‐6 signaling, to mice immediately after a 45‐min period of middle cerebral artery occlusion (MCAO). At 6 h after MCAO, IL‐6RA administration had resulted in a significant reduction in the amount of phosphorylated signal transducer and activator of transcription‐3 (Stat3) protein in the peri‐infarct area of the cortex. At 24 h after MCAO, blockade of IL‐6 signaling had led to an increase in number of apoptotic cells in the peri‐infarct area and enlargement of the size of the infarct, and it had adversely affected neurological function. These results suggest that endogenous IL‐6 plays a critical role in preventing damaged neurons from undergoing apoptosis in the acute phase of cerebral ischemia and that its role may be mediated by Stat3 activation.
Down‐regulation of Dickkopf 3, a regulator of the Wnt signalling pathway, in elderly schizophrenic subjects
Authors: Ftouh Saoussen , Akbar Mohammed T. , Hirsch Steven R. , De Belleroche Jacqueline S. 
Published: June 2005

AbstractThe aetiology of schizophrenia is complex and the pathological mechanisms involved are still not fully understood. The aim of this project was to gain insight into the underlying molecular changes occurring in schizophrenia through the analysis of gene expression. Using suppression subtractive hybridization to isolate differentially expressed genes in superior temporal cortex (BA22), we detected one prominent sequence with reduced expression in schizophrenia and represented in at least nine clones. This was then selected for further validation. This 190‐bp partial transcript showed identity to part of the Dickkopf‐3 (Dkk3) gene sequence. Differential expression was initially confirmed in BA22 by slot blot hybridization where expression was decreased by 35% (p < 0.026). These results were further authenticated in a larger panel (12 control and 11 schizophrenia cases) using SYBR Green I real‐time quantitative RT–PCR, in which a 41% decrease in expression of Dkk3 mRNA in schizophrenia was obtained (p < 0.012). Furthermore, using in situ hybridization, Dkk3 mRNA was shown to be abundantly expressed in cortical neurones, with prominent expression in layers II/III and V/VI of BA22. Dkk3 belongs to a novel family of Dkk proteins, which have been shown to be potent inhibitors of the neurodevelopmental wingless (Wnt) signalling pathway, and is therefore a putative candidate for further investigation into the aetiology of schizophrenia.
The mechanism of SR95531 inhibition at GABAA receptors examined in human α1β1 and α1β1γ2S receptors
Authors: Lindquist Catarina E. L. , Laver Derek R. , Birnir Bryndis 
Published: June 2005

AbstractWe examined the interaction of GABA and the competitive inhibitor SR95531 at human α1β1γ2S and α1β1 GABAA receptors expressed in Sf9 cells. The efficacy and potency of inhibition depended on the relative timing of the GABA and SR95531 applications. In saturating (10 mm) GABA, the half‐inhibitory concentrations of SR95531 (IC50) when coapplied with GABA to α1β1γ2S or α1β1 receptors were 49 and 210 µm for the peak and 18 and 130 µm for the plateau current, respectively. Our data are explained by an inhibition mechanism in which SR95531 and GABA bind to two sites on the receptor where the binding of GABA allows channel opening but SR95531 does not. The SR95531 affinity for both receptor types was ∼200 nm and the binding rate was found to be 10‐fold faster than that for GABA. The dual binding‐site model gives insights into the differential effects of GABA and SR95531 on the peak and plateau currents. The model predicts the effect of SR95531 on GABA currents in the synapse (GABA concentration ∼ mm) and at extrasynaptic (GABA concentration ≤ µm) sites. The IC50 (50–100 nm) for the synaptic response to SR95531 was insensitive to the GABA affinity of the receptors whereas the IC50 (50–800 nm) for extrasynaptic inhibition correlated with the GABA affinity.
Two distinct regulatory mechanisms of neurotransmitter release by phosphatidylinositol 3‐kinase
Authors: Itakura Makoto , Yamamori Saori , Kuwahara Reiko , Sekiguchi Mariko , Takahashi Masami 
Published: June 2005

AbstractRecent studies have indicated that various growth factors are involved in synaptic functions; however, the precise mechanisms remain unclear. In order to elucidate the molecular mechanisms of the growth factor‐mediated regulation of presynaptic functions, the effects of epidermal growth factor (EGF) and insulin‐like growth factor‐1 (IGF‐1) on neurotransmitter release were studied in rat PC12 cells. Brief treatment with EGF and IGF‐1 enhanced Ca2+‐dependent dopamine release in a concentration‐dependent manner. EGF activated both mitogen‐activated protein kinase (MAPK) and phosphatidylinositol 3‐kinase (PI3‐kinase) pathways, and the EGF‐dependent enhancement of DA release was suppressed by a MAPK kinase inhibitor as well as by PI3‐kinase inhibitors. In striking contrast, IGF‐1 activated the PI3‐kinase pathway but not the MAPK pathway, and IGF‐1‐dependent enhancement was suppressed by a PI3‐kinase inhibitor but not by a MAPK kinase inhibitor. The enhanced green fluorescent protein‐tagged pleckstrin homology (PH) domain of protein kinase B, which selectively binds to phosphatidylinositol 3,4‐bisphosphate and phosphatidylinositol 3,4,5‐triphosphate, was translocated to the plasma membrane after treatment with either EGF or NGF. By contrast, no significant redistribution was induced by IGF‐1. These results indicate that PI3‐kinase participates in the enhancement of neurotransmitter release by two distinct mechanisms: EGF and NGF activate PI3‐kinase in the plasma membrane, whereas IGF‐1 activates PI3‐kinase possibly in the intracellular membrane, leading to enhancement of neurotransmitter release in a MAPK‐dependent and ‐independent manner respectively.