bluuebunny/crossref_metadata_2025_split huggingface dataset:
Morphology and immunohistochemistry of efferent neurons of the goldfish corpus cerebelli
Authors: Ikenaga Takanori , Yoshida Masayuki , Uematsu Kazumasa 
Published: May 2005

AbstractIn teleosts, cerebellar efferent neurons, known as eurydendroid cells, are dispersed within the cerebellar cortex rather than coalescing into deep cerebellar nuclei. To clarify their morphology, eurydendroid cells were labeled retrogradely by biotinylated dextran amine injection into the base of the corpus cerebelli. Labeling allowed the cells to be classified into three types—fusiform, polygonal, and monopolar—depending on their somal shapes and numbers of primary dendrites. The fusiform and polygonal type cells were distributed not only in the Purkinje cell layer but also in the molecular and granule cell layers. The monopolar type cells were distributed predominantly in the Purkinje cell layer of the ventrocaudal portion of the corpus cerebelli. These results suggest that there are some functional differences between these eurydendroid cell types. The eurydendroid cells were double‐labeled by retrograde labeling and immunohistochemistry using specific antibodies against GABA, aspartate, and zebrin II. No GABA‐like immunoreactivity was detected in the retrogradely labeled eurydendroid cells. About half of retrogradely labeled cells were immunoreactive to the anti‐aspartate antibody, suggesting that some eurydendroid cells utilize aspartate as a neurotransmitter. Zebrin II reacts with cerebellar Purkinje cells but left all retrogradely labeled neurons nonreactive, although some of these were surrounded by immunopositive fibers. This relationship between the eurydendroid and Purkinje cells is similar to that between the deep cerebellar nuclei and Purkinje cells in mammals. J. Comp. Neurol. 487:300–311, 2005. © 2005 Wiley‐Liss, Inc.
μ‐opioid receptor mRNA expression in identified hypothalamic neurons
Authors: Zheng Shi‐Xi , Bosch Martha A. , Rønnekleiv Oline K. 
Published: May 2005

AbstractIt has been known for a number of years that μ‐opioid receptor agonists (e.g., morphine, β‐endorphin, and enkephalin) inhibit luteinizing hormone (LH), vasopressin (VP), and oxytocin (OT) release and stimulate prolactin secretion in rodents and primates by an action at the level of the brain. Also, electrophysiological studies have established that hypothalamic neurons, including gonadotropin‐releasing hormone (GnRH), VP, OT, β‐endorphin, and dopamine neurons, are responsive to μ‐receptor activation. Although μ‐receptor expression has been demonstrated in the hypothalamus, there have been few studies localizing these receptors in neurosecretory neurons. Therefore, we sought to document μ‐opioid receptor mRNA expression in immunocytochemically identified hypothalamic neurons. The brains from both female and male guinea pigs were examined by using in situ hybridization and immunocytochemistry. The studies revealed that μ‐receptor mRNA was expressed in different diencephalic regions including the preoptic area, the bed nuclei stria terminalis, the paraventricular nucleus thalamus, and the anterior hypothalamus, as well as the supraoptic (SON), paraventricular (PVH), ventromedial, dorsomedial, and arcuate nuclei of the hypothalamus. Importantly, μ‐opioid receptors were expressed in subpopulations of GnRH neurons (33.25 ± 4.6% and 33.6 ± 3.7% in females and males, respectively), dopamine neurons (51.7 ± 5.8% to 75.0 ± 2.6%, depending on neuronal location), β‐endorphin neurons (68.3.0 ± 4.4%), and VP neurons (41–70%, depending on neuronal location). Because μ‐opioid receptors couple via G‐proteins to activate inwardly rectifying potassium channels and to inhibit calcium channels, the presence of these receptors is likely to play a major role in directly controlling the excitability of hypothalamic neurons. J. Comp. Neurol. 487:332–344, 2005. © 2005 Wiley‐Liss, Inc.
Feedback connections to ferret striate cortex: Direct evidence for visuotopic convergence of feedback inputs
Authors: Cantone Gina , Xiao Jun , McFarlane Nardia , Levitt Jonathan B. 
Published: May 2005

AbstractInterareal feedback connections are a fundamental aspect of cortical architecture, yet many aspects of their organization and functional relevance remain poorly understood. Previous studies have investigated the topography of feedback projections from extrastriate cortex to macaque area 17. We have extended this analysis to the ferret. We made restricted injections of cholera toxin B (CTb) into ferret area 17 and mapped the distribution of retrogradely labeled cells in extrastriate cortex. In addition to extensive label spreading within area 17, we found dense cell label in areas 18, 19, and 21 and the suprasylvian cortex and sparser connections from the lateral temporal and posterior parietal cortex. We made extensive physiological assessments of magnification factors in the extrastriate visual cortex and used these measures to convert the spread of labeled cortex in millimeters into a span in degrees of visual field. We also directly measured the visuotopic extents of receptive fields in the regions containing labeled cells in cases in which we made both CTb injections and physiological recordings in the same animals; we then compared the aggregate receptive field (ARF) of the labeled region in each extrastriate area with that of the injection site. In areas 18, 19, and 21, receptive fields of cells in regions containing labeled neurons overlapped those at the injection site but spanned a greater distance in visual space than the ARF of the injection site. The broad visuotopic extent of feedback connections is consistent with the suggestion that they contribute to response modulation by stimuli beyond the classical receptive field. J. Comp. Neurol. 487:312–331, 2005. © 2005 Wiley‐Liss, Inc.
Antioxidants and an inhibitor of advanced glycation ameliorate death of retinal microvascular cells in diabetic retinopathy
Authors: Yatoh Shigeru , Mizutani Masakazu , Yokoo Tomotaka , Kozawa Tadahiko , Sone Hirohito , Toyoshima Hideo , Suzuki Seiji , Shimano Hitoshi , Kawakami Yasushi , Okuda Yukichi , Yamada Nobuhiro 
Published: May 2005

AbstractBackgroundPericyte ghosts and acellular capillaries are well known as early histological changes resulting from diabetic retinopathy. These histological changes mean that the cell death of retinal microvessels has accelerated. It was reported that apoptosis of retinal microvascular cells (RMCs) was increased in diabetic patients. Therefore, we investigated apoptosis of RMCs in Goto‐Kakizaki (GK) rats, a type 2 diabetic model, and involvement with antioxidants (a combination of vitamins C and E) or a novel inhibitor of advanced glycation, OPB‐9195.MethodsGK rats were treated with the antioxidants combination or OPB‐9195 for 36 weeks. We obtained isolated preparations of the vascular network from their retinas by trypsin digestion. Apoptosis of retinal vascular cells was detected with terminal deoxynucleotidyl transferase‐mediated dUTP nick end labeling (TUNEL) assay.ResultsWe found that apoptosis of RMCs was increased in the diabetic GK rats. Furthermore, a combination of vitamins C and E and an advanced glycation end‐products inhibitor mostly inhibited this increased apoptosis.ConclusionsWe concluded that apoptosis of RMCs was a good marker that indicates the progression of diabetic retinopathy in GK rats. Both oxidative stress and the accumulation of advanced glycation end‐products appears to promote the apoptosis of retinal microvascular cells, and antioxidants or advanced glycation end‐products inhibitors might ameliorate diabetic retinopathy. Copyright © 2005 John Wiley & Sons, Ltd.
Predicting ordinary kriging errors caused by surface roughness and dissectivity
Authors: Siska Peter P. , Goovaerts Pierre , Hung I‐Kuai , Bryant Vaughn M. 
Published: May 2005

AbstractThe magnitude of kriging errors varies in accordance with the surface properties. The purpose of this paper is to determine the association of ordinary kriging (OK) estimated errors with the local variability of surface roughness, and to analyse the suitability of probabilistic models for predicting the magnitude of OK errors from surface parameters. This task includes determining the terrain parameters in order to explain the variation in the magnitude of OK errors. The results of this research indicate that the higher order regression models, with complex interaction terms, were able to explain 95 per cent of the variation in the OK error magnitude using the least number of predictors. In addition, the results underscore the importance of the role of the local diversity of relief properties in increasing or decreasing the magnitude of interpolation errors. The newly developed dissectivity parameters provide useful information for terrain analysis. Our study also provides constructive guides to understanding the local variation of interpolation errors and their dependence on surface dissectivity. Copyright © 2005 John Wiley & Sons, Ltd.
Novel Caenorhabditis elegans unc‐119 axon outgrowth defects correlate with behavioral phenotypes that are partially rescued by nonneural unc‐119
Authors: Materi Wayne , Pilgrim David 
Published: May 2005

AbstractUNC‐119 function is necessary for the correct development of the Caenorhabditis elegans nervous system. Worms mutant for unc‐119 exhibit nervous system structural defects, including supernumerary axon branches, defasciculated nerve fibers, and choice point errors. Axons of both mechanosensory (ALM) and chemo‐ sensory (ASI) neurons have elongation defects within the nerve ring. Expressing unc‐119 cDNA in mechanosensory neurons rescues the elongation defect of ALM axons, but expression in ASI neurons does not rescue ASI axon elongation defects. Neither gross movement nor dauer larva formation defects are rescued in either case. However, expressing a construct including introns under the control of the same promoters results in substantial rescue of phenotypic defects. In these cases reporter expression expands to tissues outside those specified by the promoter, notably into head muscles. Surprisingly, expressing an unc‐119 cDNA construct under the control of a muscle‐specific promoter fully rescues the dauer formation defect and substantially rescues movement. Thus, although UNC‐119 normally acts in a cell‐autonomous fashion, the cell‐nonautonomous rescue of neural function suggests that it either acts at the cell surface or that it can be transported into the cell from the extracellular environment and play its normal role. genesis 42:104–116, 2005. © 2005 Wiley‐Liss, Inc.
Robust ascertainment‐adjusted parameter estimation
Authors: Noh Maengseok , Lee Youngjo , Pawitan Yudi 
Published: May 2005

AbstractNonrandom ascertainment is commonly used in genetic studies of rare diseases, since this design is often more convenient than the random‐sampling design. When there is an underlying latent heterogeneity, Epstein et al. ([2002] Am. J. Hum. Genet. 70:886–895) showed that it is possible to get unbiased or consistent estimation of population parameters under ascertainment adjustment, but Glidden and Liang ([2002] Genet. Epidemiol. 23:201–208) showed in a simulation study that the resulting estimates are highly sensitive to misspecification of the latent components. To overcome this difficulty, we consider a heavy‐tailed model for latent variables that allows a robust estimation of the parameters. We describe a hierarchical‐likelihood approach that avoids the integration used in the standard marginal likelihood approach. We revisit and extend the previous simulation, and show that the resulting estimator is efficient and robust against misspecification of the distribution of latent variables.Genet. Epidemiol. © 2005 Wiley‐Liss, Inc.
Excitotoxic oligodendrocyte death and axonal damage induced by glutamate transporter inhibition
Authors: Domercq María , Etxebarria Estibaliz , Pérez‐Samartín Alberto , Matute Carlos 
Published: May 2005

AbstractGlutamate uptake is crucial to terminate glutamate signaling and to prevent excitotoxicity. The present study describes the expression of functional glutamate transporters GLAST and GLT‐1 in oligodendrocytes by means of electrophysiology, uptake assays, and immunocytochemistry. Inhibition of glutamate uptake, both in oligodendrocyte cultures and in isolated optic nerves, increases glutamate levels and causes oligodendrocyte excitotoxicity, which is prevented by alpha‐amino‐3‐hydroxy‐5‐methylisoxazole‐4‐propionic acid (AMPA) and kainate receptor antagonists. Furthermore, glutamate transporter inhibitors or antisense oligonucleotides applied onto the optic nerve in vivo lead to oligodendroglial loss, massive demyelination, and severe axonal damage. Overall, these results demonstrate that the integrity of oligodendrocytes and white matter depends on proper glutamate transporter function. Deregulated transporter activity may contribute to acute and chronic white matter damage. © 2005 Wiley‐Liss, Inc.
Evidence for creatine biosynthesis in Müller glia
Authors: Nakashima Toshihisa , Tomi Masatoshi , Tachikawa Masanori , Watanabe Masahiko , Terasaki Tetsuya , Hosoya Ken‐ichi 
Published: May 2005

AbstractIn high‐energy metabolic tissues like the retina, creatine may play an important role in energy storage and in transmission of phosphate‐bound energy substrates. To prove this, we investigated creatine synthesis in Müller glia. We also characterized the localization of the creatine synthetic enzyme, S‐adenosyl‐L‐methionine:N‐guanidinoacetate methyltransferase (GAMT) in the retina. Reverse transcription‐polymerase chain reaction analysis revealed that L‐arginine:glycine amidinotransferase and GAMT mRNAs were expressed in the retina and the Müller cell line, TR‐MUL5. [14C]Creatine was detected after incubation of isolated rat retina or TR‐MUL5 cells with [14C]glycine, L‐arginine and L‐methionine, suggesting creatine synthesis in Müller glia. Western blot analysis also revealed expression of GAMT protein in the rat retina and TR‐MUL5 cells. Furthermore, confocal immunofluorescent microscopy of dual‐labeled rat retinal sections demonstrated co‐localization of GAMT with glutamine synthetase. Taken together, the results of the present study indicate creatine synthesis in Müller glia, implying an important role of creatine in energy metabolism in the retina. © 2005 Wiley‐Liss, Inc.
Tenascin C induces a quiescent phenotype in cultured adult human astrocytes
Authors: Holley Janet E. , Gveric Djordje , Whatmore Jacqueline L. , Gutowski Nicholas J. 
Published: May 2005

AbstractAstrocytic scar formation occurs subsequent to brain and spinal cord injury and impedes repair. The exact mechanisms of scar formation have yet to be elucidated but it is known that astrocytes within the scar have a different antigenic phenotype from normal or reactive astrocytes. Astrocyte cell culture offers a suitable system to identify factors that induce the scar phenotype as well as factors that reverse this process and that may help identify therapeutic strategies to treat astrogliosis. However, when placed in standard culture conditions, astrocytes become activated/reactive and express molecules characteristic of scar tissue in vivo. In the present study, we made use of this phenomenon to identify culture conditions that change the activated phenotype of cultured astrocytes into one characteristic of normal quiescent astrocytes. In particular, we examined the effect of extracellular matrix (ECM) proteins found in the human brain, on the phenotype of human adult astrocytes. Significantly fewer astrocytes expressed scar properties when grown on tenascin‐C (TN‐C) than those cultured on other ECM proteins or poly‐L‐lysine‐coated dishes. TN‐C also significantly reduced the proliferation rate of the astrocytes in vitro. In addition, further manipulation of culture conditions induced partial astrocyte reactivation. Our findings suggest that astrocytes grown on TN‐C revert to a quiescent, nonactivated state that is partially reversible. This raises the possibility that therapeutic strategies aimed at manipulating TN‐C levels during CNS injury may help reduce astrocytic scarring. © 2005 Wiley‐Liss, Inc.
Functions and distribution of voltage‐gated sodium and potassium channels in mammalian schwann cells
Authors: Chiu S. Y. 
Published: May 2005

AbstractRecent patch‐clamp studies on freshly isolated mammalian Schwann cells suggest that voltage‐gated sodium and potassium channels, first demonstrated in cells under culture conditions, are present in vivo. The expression of these channels, at least at the cell body region, appears to be dependent on the myelinogenic and proliferative states of the Schwann cell. Specifically, myelin elaboration is accompanied by a down regulation of functional potassium channel density at the cell body. One possibility to account for this is a progressive regionalization of ion channels on a Schwann cell during myelin formation. In adult myelinating Schwann cells, voltage‐gated potassium channels appear to be localized at the paranodal region. Theoretical calculations have been made of activity‐dependent potassium accumulations in various compartments of a mature myelinated nerve fibre; the largest potassium accumulation occurs not at the nodal gap but rather at the adjacent 2–4 μm length of periaxonal space at the paranodal junction. Schwann cell potassium channels at the paranode may contribute to ionic regulation during nerve activities.
Neurons and astrocytes influence the development of purified o‐2a progenitor cells
Authors: Dutly F. , Schwab M. E. 
Published: May 2005

AbstractTo investigate the possible role of neurons and astrocytes for oligodendrocyte development we prepared a pure population of precursor cells positive for the precursor marker GD3 with the help of fluorescence‐activated cell sorting (FACS). Large numbers of highly purified cells were obtained from postnatal day 1 rat brainstems and cultured in different media and sera, and in conditioned media.As described in the literature for optic nerve O‐2A progenitors, GD3‐sorted brainstem cells cultured in medium containing 10% fetal calf serum (FCS) acquired a star‐shaped morphology and differentiated into GD3‐ and GFAP‐positive type‐2 astrocytes. On the other hand, in serum‐free medium, most of the cells differentiated into oligodendrocytes (O1‐/galactocerebroside‐positive).Sensory neuron conditioned media promoted survival and proliferation of the precursor cells. The spontaneous differentiation of progenitor cells into oligodendrocytes was retarded by the mitogen. Antibodies against platelet‐derived growth factor (PDGF) completely blocked the mitotic effect and allowed spontaneous oligodendrocyte differentiation to occur.Cultured astrocytes also secreted PDGF as a mitogen. However, postnatal astrocytes also released a potent signal promoting oligodendrocyte differentiation. The type of factor(s) released depended on the age of the astrocytes, since only conditioned medium of postnatal but not of embryonic astrocytes promoted oligodendrocyte differentiation, suggesting that astrocyte maturation directly influences oligodendrocyte differentiation. Different concentrations of PDGF could not reproduce this differentiation‐inducing effect.This study suggests that interactions between O‐2A progenitor cells, neurons, and astrocytes could be required to regulate and complete the oligodendrocyte developmental pathway. Astrocytes, themselves possibly under neuronal influences, might regulate first the proliferation of the precursor cells, and, later in development, the differentiation into mature oligodendrocytes or type‐2 astrocytes.
Phorbol‐12‐myristate‐13‐acetate (PMA) and inhibitors of protein kinase C alter glial fibrillary acidic protein (GFAP) mRNA levels
Authors: Sharma Nishi , Norman‐O'guin Kathleen , Shafit‐Zagardo Bridget 
Published: May 2005

AbstractGlial fibrillary acidic protein (GFAP) mRNA levels in the human astrocytoma line U‐373MG were examined to explore further the effects of agents that regulate protein kinase C. U‐373MG cells exhibit a biphasic change in steady‐state GFAP mRNA in the presence of the phorbol ester phorbol‐12‐myristate‐13‐acetate (PMA). Short‐term treatment with PMA results in increased GFAP mRNA, and long‐term treatment results in decreased GFAP mRNA. Nuclear run‐off experiments demonstrate that the PMA‐induced decrease in GFAP mRNA levels is not at the level of GFAP gene transcription. PMA exerts its effect in the presence of protein synthesis inhibitors, demonstrating that de novo protein synthesis is not required for the PMA‐induced changes in GFAP mRNA. Staurosporine, a protein kinase C inhibitor, reduces GFAP mRNA expression in a dose‐dependent manner; in the presence of PMA the effect is additive. By contrast HA1004, an inhibitor of cAMP‐dependent protein kinase, is not inhibitory to GFAP steady‐state mRNA. Total protein kinase C activity was determined to be 2,398.8 ± 94.3 pmol/min/mg protein, with most of the activity in the cytosol. Short‐term PMA treatment results in the translocation of the cytosolic protein kinase C activity to the membrane. Long‐term PMA treatment results in a decrease in total protein kinase C activity indicating that downregulation occurs. These studies demonstrate that in the U‐373MG cells, protein kinase C inhibitors and long treatment with PMA result in a decrease in steady‐state GFAP mRNA.
Rumpshaker: An X‐linked mutation causing hypomyelination: Developmental differences in myelination and glial cells between the optic nerve and spinal cord
Authors: Fanarraga M. L. , Griffiths I. R. , McCulloch M. C. , Barrie J. A. , Kennedy P. G. E. , Brophy P. J. 
Published: May 2005

AbstractThe X‐linked mutation rumpshaker (rsh), which is probably an allele of jimpy (jp), causes hypomyelination in the CNS of mice. This study examines the developmental expression of the morphology, glial cells, and immunostaining of myelin proteins in the optic nerve and spinal cord. The optic nerve contains varying numbers of amyelinated and myelinated fibres. The majority of such sheaths are of normal thickness whereas in the spinal cord most axons are associated with a disproportionately thin sheath which changes little in thickness during development. In the optic nerve glial cell numbers are elevated in mutants during early and peak myelination but then fall slightly below normal in adults. In contrast, the number of glial cells is consistently elevated after 16 days of age in the spinal cord. The majority of the alterations to total glial cells are due to corresponding changes in the oligodendrocyte population. Immunostaining intensity is somewhat reduced for myelin basic protein (MBP) and the C‐terminal common to proteolipid protein (PLP) and DM‐20 and profoundly decreased for the PLP‐specific peptide. Glial fibrillary acidic protein (GFAP) is increased in rsh. It is probable that some of the variation in myelination between optic nerve and cord in rsh is related to the difference in axon diameter in the two locations, as there are adequate numbers of oligodendrocytes at the time of myelination. However, the effect of the mutation on cell development in the brain and the spinal cord may be different. The immunostaining indicates a marked deficiency in PLP in myelin but suggests that DM‐20 levels may be relatively normal. rsh shows several major differences from jp and other X‐linked myelin mutants, particularly in relation to oligodendrocyte numbers, and will be useful to elucidate the role of the PLP gene in influencing oligodendrocyte differentiation and survival.