bluuebunny/crossref_metadata_2025_split huggingface dataset:
Genetic fate mapping of Olig2 progenitors in the injured adult cerebral cortex reveals preferential differentiation into astrocytes
Authors: Tatsumi Kouko , Takebayashi Hirohide , Manabe Takayuki , Tanaka Kenji F. , Makinodan Manabu , Yamauchi Takahira , Makinodan Eri , Matsuyoshi Hiroko , Okuda Hiroaki , Ikenaka Kazuhiro , Wanaka Akio 
Published: September 2008

AbstractOlig2 is a basic helix‐loop‐helix (bHLH) transcription factor essential for development of motoneurons and oligodendrocytes. It is known that Olig2+cells persist in the central nervous system (CNS) from embryonic to adult stages and that the number of Olig2+progenitors increases in the injured adult CNS. Recent studies have demonstrated an inhibitory action of Olig2 on neurogenesis in adult CNS, but the fate of Olig2+cells in the injured state remains largely unknown. To trace directly the fate of Olig2 cells in the adult cerebral cortex after injury, we employed the CreER/loxP system to target theolig2locus. In this genetic tracing study, green fluorescent protein (GFP) reporter‐positive cells labeled after cryoinjury coexpressed glial fibrillary acidic protein (GFAP), an astrocytic marker. Electron microscopy also showed that GFP+cells have the ultrastructural characteristics of astrocytes. Furthermore, GFP+cells labeled before injury, most of which had been NG2 cells, also produced bushy astrocytes. Here we show direct evidence that Olig2+cells preferentially differentiate into astrocytes, which strongly express GFAP, in response to injury in the adult cerebral cortex. These results suggest that reactive astrocytes, known to be the main contributors to glial scars, originate, at least in part, from Olig2+cells. © 2008 Wiley‐Liss, Inc.
Developmental regulation of metabotropic glutamate receptor 1 splice variants in olfactory bulb mitral cells
Authors: Bovolin P. , Bovetti S. , Fasolo A. , Katarova Z. , Szabo G. , Shipley M.T. , Margolis F.L. , Puche A.C. 
Published: September 2008

AbstractAlternative splicing of the metabotropic glutamate receptor 1 (mGluR1) receptor gene generates two major receptor isoforms, mGluR1a and mGluR1b, differing in intracellular function and distribution. However, little is known on the expression profiles of these variants during development. We examined the mRNA expression profile of mGluR1a/b in microdissected layers and acutely isolated mitral cells in the developing mouse olfactory bulb. This analysis showed that the two mGluR1 variants are differentially regulated within each bulb layer. During the first postnatal week, the mGluR1a isoform replaces GluR1b in the microdissected mitral cell layer (MCL) and in isolated identified mitral cells, coinciding with a developmental epoch of mitral cell dendritic reorganization. Although mGluR1a mRNA is expressed at high levels in both the adult external plexiform layer (EPL) and MCL, Western blotting analysis reveals a marked reduction of the mGluR1a protein in the MCL, where mitral cell bodies are located, and strong labeling in the EPL, which contains mitral cell dendrites. This suggests that there is increased dendritic trafficking efficiency of the receptor in adult. The temporal and spatial shift in mGluR1b/a expression suggests distinct roles of the mGluR1 isoforms, with mGluR1b potentially involved in the early mitral cell maturation and mGluR1a in dendritic and synapse function. © 2008 Wiley‐Liss, Inc.
M4 muscarinic receptors are involved in modulation of neurotransmission at synapses of Schaffer collaterals on CA1 hippocampal neurons in rats
Authors: Sánchez Gonzalo , de Oliveira Alvares Lucas , Oberholzer María Victoria , Genro Bruna , Quillfeldt Jorge , da Costa Jaderson Costa , Cerveñansky Carlos , Jerusalinsky Diana , Kornisiuk Edgar 
Published: September 2008

AbstractAll five subtypes of muscarinic acetylcholine receptors (mAChR; M1–M5) are expressed in the hippocampus, where they are involved both in cognitive functions and in synaptic plasticity, such as long‐term potentiation (LTP). Muscarinic toxins (MTs) are small proteins from mamba snake venoms that display exquisite discrimination between mAChRs. MT1 acts as an agonist at M1 and an antagonist at M4 receptors, with similar affinities for both. MT3, the most selective antagonist available for M4 receptors, infused into the CA1 region immediately after training caused amnesia in the rat, indicating the participation of M4 receptors in memory consolidation. Our goal was to investigate the participation of M4 receptor in neurotransmission at the hippocampal Schaffer collaterals‐CA1 synapses. Two different preparations were used: 1) field potential recordings in freshly prepared rat hippocampal slices with high‐frequency stimulation to induce potentiation and 2) whole‐cell voltage clamp in cultured hippocampal organotypic slices with paired stimuli. In preparation 1, a dose of MT3 that was previously shown to cause amnesia blocked LTP; the nonselective antagonist scopolamine blocked LTP without affecting basal transmission, although it was depressed with higher concentration. In preparation 2, basal transmission was decreased and LTP induction was prevented by an MT3 concentration that would bind mainly to M4 receptors. Although M1 receptors appeared to modulate transmission positively at these excitatory synapses, M1 activation concomitant with M4 blockade (by MT1) only allowed a brief, short‐term potentiation. Accordingly, M4 blockade by MT3 strongly supports a permissive role of M4 receptors and suggests their necessary participation in synaptic plasticity at these synapses. © 2008 Wiley‐Liss, Inc.
1,25‐Dihydroxyvitamin D3 administration to 6‐hydroxydopamine‐lesioned rats increases glial cell line‐derived neurotrophic factor and partially restores tyrosine hydroxylase expression in substantia nigra and striatum
Authors: Sanchez Begoña , Relova Jose L. , Gallego Rosalia , Ben‐Batalla Isabel , Perez‐Fernandez Roman 
Published: September 2008

AbstractIt has previously been demonstrated that 1,25‐dihydroxyvitamin D3 [1,25(OH)2D3] administration, whether in cell cultures or in vivo to rats, increases glial cell line‐derived neurotrophic factor (GDNF) expression levels, suggesting that this hormone may have beneficial effects in neurodegenerative disorders. This study was carried out to explore the effects of 1,25(OH)2D3 administration in a 6‐OHDA‐lesioned rat model of Parkinson's disease on GDNF and tyrosine hydroxylase (TH) expression in substantia nigra (SN) and striatum. Two groups of animals received 1,25(OH)2D3 intraperitoneally, the first group 7 days before the unilateral injection of 6‐OHDA into the medial forebrain bundle (MFB) and the second group 21 days (days 21–28) after the unilateral injection of 6‐OHDA. Animals of both groups were sacrificed on day 28. In addition, two other groups received a unilateral injection of either saline or 6‐OHDA into the MFB. Rats were killed, and the SN and striatum were then removed for GDNF and TH determination. Striatal GDNF protein expression was increased on the ipsilateral with respect to the contralateral side after 6‐OHDA injection alone as well as in 1,25(OH)2D3‐treated rats before or after 6‐OHDA administration. As expected, 6‐OHDA injection induced an ipsilateral decrease in TH‐immunopositive neuronal cell bodies and axonal terminals in the SN and striatum. However, treatment with 1,25(OH)2D3 before and after 6‐OHDA injection partially restored TH expression in SN. These data suggest that 1,25(OH)2D3 may help to prevent dopaminergic neuron damage. © 2008 Wiley‐Liss, Inc.
Seizures increase importin‐β1 expression in NG2+ cells in the rat hippocampus
Authors: Brilli Elisa , Scali Manuela , Casarosa Simona , Köhler Matthias , Bozzi Yuri 
Published: September 2008

AbstractImportins, also called karyopherins, belong to a large family of proteins involved in cytoplasm‐to‐nucleus transport. Transport machinery generally involves a complex formed by two different importin subtypes (α and β). Both α and β importins are expressed in the brain, and their expression and localization is regulated by physiological neuronal activity. Little is known about regulation of importin expression in brain pathological conditions. Here we studied the expression of importin β1 (impβ1) in the rat hippocampus after acute and chronic seizures induced by the glutamate agonist kainic acid (KA). The overall content of impβ1 mRNA and protein did not change after acute KA seizures. However, acute KA seizures rapidly induced the translocation of impβ1 protein from the cytoplasm to the nucleus in pyramidal CA1 neurons. KA‐induced impβ1 translocation was prevented by the NMDA (N‐methyl‐D‐aspartic acid) receptor blocker MK‐801. After chronic seizures, the overall levels of impβ1 mRNA and protein did not change in the whole hippocampus. Immunohistochemistry revealed a massive loss of impβ1‐positive neurons in pyramidal layers (that degenerated after KA), whereas an increased number of impβ1‐positive cells was detected in the stratum radiatum of rats with chronic seizures compared with control animals. Double‐labeling experiments identified these cells as glial cells expressing the chondroitin sulfate proteoglycan NG2 (neuron/glial antigen 2), a glial subtype recently shown to regulate hippocampal neuron excitability. These data show a differential regulation of impβ1 expression after acute and chronic seizure activity in the rat hippocampus. © 2008 Wiley‐Liss, Inc.
Protection against kainate neurotoxicity by ginsenosides: Attenuation of convulsive behavior, mitochondrial dysfunction, and oxidative stress
Authors: Shin Eun‐Joo , Jeong Ji Hoon , Kim A‐Young , Koh Young Ho , Nah Seung‐Yeoul , Kim Won‐Ki , Ko Kwang Ho , Kim Hyun Ji , Wie Myung‐Bok , Kwon Yong Soo , Yoneda Yukio , Kim Hyoung‐Chun 
Published: September 2008

AbstractWe previously demonstrated that kainic acid (KA)‐mediated mitochondrial oxidative stress contributed to hippocampal degeneration and that ginsenosides attenuated KA‐induced neurotoxicity and neuronal degeneration. Here, we examined whether ginsenosides affected KA‐induced mitochondrial dysfunction and oxidative stress in the rat hippocampus. Treatment with ginsenosides attenuated KA‐induced convulsive behavior dose‐dependently. KA treatment increased lipid peroxidation and protein oxidation and decreased the reduced glutathione/oxidized glutathione (GSH/GSSG) ratio to a greater degree in the mitochondrial fraction than in the hippocampal homogenate. KA treatment resulted in decreased Mn‐superoxide dismutase expression anddiminished the mitochondrial membrane potential. Furthermore, KA treatment increased intramitochondrial Ca2+ and promoted ultrastructural degeneration in hippocampal mitochondria. Treatment with ginsenosides dose‐dependently attenuated convulsive behavior and the KA‐induced mitochondrial effects. Protection appeared to be more evident in mitochondria than in tissue homogenates. Collectively, the results suggest that ginsenosides prevent KA‐induced neurotoxicity by attenuating mitochondrial oxidative stress and mitochondrial dysfunction. © 2008 Wiley‐Liss, Inc.
Guanosine improves motor behavior, reduces apoptosis, and stimulates neurogenesis in rats with parkinsonism
Authors: Su Caixin , Elfeki Nada , Ballerini Patrizia , D'Alimonte Iolanda , Bau Christian , Ciccarelli Renata , Caciagli Francesco , Gabriele Joseph , Jiang Shucui 
Published: September 2008

AbstractParkinson's disease (PD) is characterized by progressive degeneration of dopaminergic neurons in the substantia nigra pars compacta (SNc) caused by an abnormal rate of apoptosis. Endogenous stem cells in the adult mammalian brain indicate an innate potential for regeneration and possible resource for neuroregeneration in PD. We previously showed that guanosine prevents apoptosis even when administered 48 hr after the toxin 1‐methyl‐4‐phenylpyridinium (MPP+). Here, we induced parkinsonism in rats with a proteasome inhibitor. Guanosine treatment reduced apoptosis, increased tyrosine hydroxylase–positive dopaminergic neurons and expression of tyrosine hydroxylase in the SNc, increased cellular proliferation in the SNc and subventricular zone, and ameliorated symptoms. Proliferating cells in the subventricular zone were nestin‐positive adult neural progenitor/stem cells. Fibroblast growth factor‐2‐expressing cells were also increased by guanosine. Thus, guanosine protected cells from apoptosis and stimulated “intrinsic” adult progenitor/stem cells to become dopaminergic neurons in rats with proteasome inhibitor–induced PD. The cellular/molecular mechanisms underlying these effects may open new avenues for development of novel therapeutics for PD. © 2008 Wiley‐Liss, Inc.
Recruitment of pericytes and astrocytes is closely related to the formation of tight junction in developing retinal vessels
Authors: Kim Jeong Hun , Kim Jin Hyoung , Yu Young Suk , Kim Dong Hun , Kim Kyu‐Won 
Published: September 2008

AbstractDuring retinal development, retinal vascularization begins in the inner retinal layer and sprouts radially from the optic nerve to reach the periphery of the retina. Subsequently, retinal vessels sprout into the deep retinal layer to form three parallel of the nerve fiber layer and two plexiform layers. In this process, endothelial cells are closely related to astrocytes and pericytes with strict chronological order. Here, we provide that the recruitment of pericytes and astrocytes to vascular tube of endothelial cells is closely associated with the formation of tight junction in developing retinal vessels. At P4, endothelial cells of retinal vessels behind the invading front directly contact to pericytes, but not to foot processes of astrocytes, where ZO‐1 was already weakly immunoreactive along retinal endothelial cells. With the progression of retinal development, foot processes of astrocytes are gathered around retinal vessels and the maturation of tight junction in endothelial cells is clearly defined, which was temporally and spatially accordant to the expression of a tight junction protein, ZO‐1. In addition, tight junction could be formed with contact of pericytes to endothelial cells without the prominent ensheathment of astrocytic foot processes, which coincided with the appearance of a tight junction protein, ZO‐1. Therefore, these data demonstrate that the tight junction of endothelial cells in the blood–retina barrier could be developed by cellular interactions between pericytes, astrocytes, and endothelial cells. Moreover, ZO‐1 as well as occludin or claudin might demonstrate the tightness of blood–retina barrier in developing retina. © 2008 Wiley‐Liss, Inc.
Interaction between protein kinase C and protein kinase A can modulate transmitter release at the rat neuromuscular synapse
Authors: Santafé M. M. , Garcia N. , Lanuza M. A. , Tomàs M. , Tomàs J. 
Published: September 2008

AbstractWe used intracellular recording to investigate the functional interaction between protein kinase C (PKC) and protein kinase A (PKA) signal transduction cascades in the control of transmitter release in the neuromuscular synapses from adult rats. Our results indicate that: 1) PKA and PKC are independently involved in asynchronous release. 2) Evoked acetylcholine (ACh) release is enhanced with the PKA agonist Sp‐8‐BrcAMP and the PKC agonist phorbol ester (PMA). 3) PKA has a constitutive role in promoting a component of normal evoked transmitter release because, when the kinase is inhibited with H‐89, the release diminishes. However, the PKC inhibitor calphostin C (CaC) does not affect ACh release. 4) PKA regulates neurotransmission without PKC involvement because, after PMA or CaC modulation of the PKC activity, coupling to the ACh release of PKA can normally be stimulated with Sp‐8‐BrcAMP or inhibited with H‐89. 5) After PKA inhibition with H‐89, PKC stimulation with PMA (or inhibition with CaC) does not lead to any change in evoked ACh release. However, in PKA‐stimulated preparations with Sp‐8‐BrcAMP, PKC becomes tonically active, thus potentiating a component of release that can now be blocked with CaC. In normal conditions, therefore, PKA was able to modulate ACh release independently of PKC activity, whereas PKA stimulation caused the PKC coupling to evoked release. In contrast, PKA inhibition prevent PKC stimulation (with the phorbol ester) and coupling to ACh output. There was therefore some dependence of PKC on PKA activity in the fine control of the neuromuscular synaptic functionalism and ACh release. © 2008 Wiley‐Liss, Inc.
Differential alteration of hippocampal excitatory synaptic transmission by cannabinoid ligands
Authors: Bajo Michal , Roberto Marisa , Schweitzer Paul 
Published: September 2008

AbstractCannabinoid compounds affect synaptic activity and plasticity in numerous brain areas by activating CB1 receptors (CB1). In hippocampus, varying results have been obtained on the extent and site of cannabinoid actions on excitatory transmission, ranging from no effect to complete obliteration of synaptic responses. Here we used the rat hippocampal slice preparation to study and compare the effect of various synthetic and endogenous CB1 ligands on excitatory synaptic transmission. The full CB1 agonist WIN55212‐2 (WIN2) greatly decreased excitatory synaptic transmission by 62%. The effect of WIN‐2 was concentration dependent (EC50 of 200 nM) and completely prevented by CB1 antagonists. The nondegradable partial CB1 agonist R1‐methanandamide (mAEA) decreased transmission by 25% and the endocannabinoids 2‐arachidonylglycerol (2‐AG) and anandamide (AEA) had no significant effect. The action of AEA was improved by inhibiting its degradation but not its transport. The effect of 2‐AG was enhanced upon inhibition of COX‐2 but remained unchanged with blockade of monoacylglycerol lipase (MAGL). The observed effects were prevented by CB1 antagonists regardless of the ligand used, and paired‐pulse paradigms pointed to presynaptic mechanisms of cannabinoid action. Our results show that cannabinoid effects on neuronal activity differ widely according to the CB1 ligand used. We observed large differences between full (synthetic) and partial (endogenous) CB1 agonists in altering synaptic transmission, notably because of the involvement of active degradation mechanisms. © 2008 Wiley‐Liss, Inc.
Work and non‐work correlates of illness and behaviour in male and female Swedish white collar workers
Authors: Karasek Robert , Gardell Bertil , Lindell Jan 
Published: September 2008

AbstractFour broad classes of dependent variables (psychological strain, physical illness symptoms, health‐related behaviour and social participation) were associated with eleven categories of stressors and stress moderators from work and family life, using multiple logistic regression analysis for a random sample of 8700 full‐time male and female members of T.C.O., a major Swedish white‐collar labour federation (covering 25 per cent of the Swedish labour force). Our goal was to find broad patterns of associations by comparing relative magnitudes of effects for (a) stressors and stress moderators; (b) work and family activities, and (c) males and females.Fifty per cent of the associations between environmental factors and dependent variables were significant in the predicted direction at the 5 per cent level. However, only 5 per cent of the associations are as strong, for example, as average smoking/heart disease associations. Our primary conclusion is that job factors are the next strongest set of predictors of health and behaviour after age. Job factors are stronger than family factors for both men and women; proportionally increasing the explained variance by over 60 per cent versus roughly 20 per cent for family factors (over the 25 per cent of explanation due to demographic factors). The overall pattern of stressor/outcome associations is quite similar for men and women, although both job/outcome and family burden/outcome associations are stronger for women than for men. We failed to find a clear linkage between particular stressors and particular physical illnesses. Among the job factors, control and work load have the strongest associations; with the former predicting behaviour patterns and job satisfaction (along with social support), and the latter predicting mental strain symptoms. Family problems are associated with increased health risks (stronger for men) and family responsibilities and constraints affect health behaviour (stronger for women). Job satisfaction is the most successfully predicted outcome in the study, and is similarly affected for men and women.
Motivations of aspiring male and female entrepreneurs
Authors: Cromie Stanley 
Published: September 2008

AbstractThis study examines the motives that stimulate individuals into becoming business proprietors. More specifically, it aims to discover if entrepreneurs have multiple motives for creating their enterprises, if non‐economic motives predominate over economic ones, and if men and women have similar reasons for business founding.Results, based on personal interviews with 35 men and 34 women, indicate that both genders have a variety of reasons for founding and that women, as well as men, are primarily motivated by autonomy, achievement, a desire for job satisfaction and other non‐economic rewards. A desire to make money is not, however, an unimportant motive.Turning to differences in motives we find that women are less concerned with making money and often choose business proprietorship as a result of career dissatisfaction. They also see entrepreneurship as a means of meeting simultaneously their own career needs and the needs of their children.
Kohlenhydratstoffwechsel bei Bacillus subtilis: Radiorespiratorische Untersuchung des Glucosemetabolismus
Authors: Riedel K. 
Published: September 2008

AbstractDer anteilige Abbau der Glucose über den EMPAbkürzungen: EMP EMBDEN‐MEYERHOF‐PARNAS‐WEG (Glykolyse), HMP Hexosemonophosphatweg. HMPO oxydativer Teil des HMP, HMPN, nichtoxydativer HMP‐Teil, ED ENTNER‐DOUDOROFF‐WEG, TG Trockengewicht
sowie über den oxydativen und nichtoxy‐dativen HMP bei Bacillus subtilis wurde erfaßt durch die Bildung von radioaktiv markiertem CO2 und der Markierung der RNS nach Verfütterung von Glucose‐1‐C14 und Glucose‐6‐C14. Der Nachweis des Glucoseabbaus sowohl über den oxydativen als auch über den nichtoxydativen Teil des HMP wurde durch die Radiomarkierung der RNS erbracht und, hierauf aufbauend, eine Methode zur Berechnung dieser beiden Abbauwege entwickelt. Unter den Bedingungen nichtwachsender Kulturen werden über den EMP 62%, oxydativen HMP 20% und nichtoxydativen HMP 18% abgebaut.
Daily observations: Necessity, ritual or imposition?
Authors: Revfeim K. J. A. 
Published: September 2008

AbstractThe cost of paid observers and inconvenience to voluntary observers brings into question the necessity for climate observations on weekends and public holidays. Proper interpretation of extreme or accumulated values, carried through to observations on the next workday, shows negligible effect on derived characteristics compared with regular daily observations. Statistical methods are given for parameter estimation, where some of the values are specified as data bounds. Monthly characteristics are estimated for a 123‐year rainfall record and 59‐year temperature record to validate the procedures.