bluuebunny/crossref_metadata_2025_split huggingface dataset:
Induction of astrocyte glutamine synthetase activity by the lathyrus toxin β‐N‐oxalyl‐L‐α,β‐diaminopropionic acid (β‐L‐ODAP)
Authors: Miller Stephan , Nunn Peter B. , Bridges Richard J. 
Published: January 2005

Abstractβ‐N‐Oxalyl‐L‐α,β‐diaminopropionic acid (β‐L‐ODAP) is thought to be the causative agent in lathyrism due to its neuroexcitatory and neurotoxic properties. We have recently reported that β‐L‐ODAP is also gliotoxic at high concentrations (Bridges et al.: Brain Res 561:262, 1991). Evidence is now presented that low, subgliotoxic concentrations of β‐L‐ODAP may alter the ability of astrocytes to regulate glutamate concentrations in the CNS by increasing astrocyte glutamine synthetase activity. When astrocytes cultured from rat cortex were exposed to 100 μM β‐L‐ODAP for 24 h, the resulting glutamine synthetase activity was 155% of control levels. This effect was enantiomer and isomer‐specific, dose‐dependent, and required protein translation as the induction was blocked with cycloheximide. The effect of β‐L‐ODAP on glutamine synthetase was not mimicked by α‐amino‐3‐hydroxy‐5‐methyl‐isoxazole‐4‐propionate (AMPA) or kainate, suggesting that the induction was not transduced solely through activation of cell surface non‐N‐methyl‐D‐aspartate (NMDA) glutamate receptors. An intracellular site of action of β‐L‐ODAP is proposed because its effect on glutamine synthetase activity could be blocked by the amino acid uptake blocker dihydrokainate.
Characterization of stretch‐activated ion channels in cultured astrocytes
Authors: Islas Leon , Pasantes‐Morales Herminia , Sanchez Jorge A. 
Published: January 2005

AbstractThe presence of a stretch‐activated channel in rat cerebellar astrocytes in culture is described. This stretch‐sensitive channel is K+ ‐selective and its open probability increases with suction following a Boltzmann‐like distribution with half activation at 45 mm Hg. Kinetic analysis of the single‐channel data indicated that there are two open and two closed states and that the shortest time constants of both open and closed states are the most sensitive to suction. A symmetrical two‐barrier‐one‐site permeation model can quantitatively describe the inward rectification of the single‐channel current to voltage relations. It is suggested that this stretch‐activated channel plays a role in the regulatory volume response of astrocytes to hyposmotic conditions. © 1993 Wiley‐Liss, Inc.
Changes in ultrastructure and voltage‐dependent currents at the glia limitans of the frog optic nerve following retinal ablation
Authors: Blanco Rosa E. , Marrero Hector , Orkand Paula M. , Orkand Richard K. 
Published: January 2005

AbstractThe surface of the frog optic nerve consists of astrocytic processes separated by narrow extracellular clefts underlying a pial sheath of loose connective tissue. Macroscopic voltage dependent currents can be recorded from this surface using the loose patch‐clamp technique. In this study the changes in ultrastructure and voltage dependent Na currents have been studied for up to 1 year following removal of the retina. During the first 1–4 weeks, many of the myelinated and unmyelinated axons of the retinal ganglion cells degenerate, and the debris is phagocytosed by macrophages and glial cells. However, some morphologically intact axons remain even 12 weeks after surgery. Finally, after 16 weeks all the axons have disappeared, leaving a nerve consisting only of glial cells, some of which contain phagosomes. At 40–52 weeks after enucleation, the nerve persists, at 20–40% of the normal diameter, consisting mostly of normal looking astrocytes. The amplitude of the voltage dependent Na currents recorded from nerves during the first 1–4 weeks after enucleation, with the pial sheath intact, decreases by about 50%. After 8 weeks, the Na current recorded from the surface is about 30% of control. At 16–52 weeks after removal of the retina, when there are no intact axons, the Na current is reduced by 90%. If, however, the pial sheath is stripped away, the Na currents recorded from the glial surface are 40–50% of control during this same 16‐ to 52‐week period, suggesting that in the all‐glia nerve, the currents are shunted by the relatively thicker pial sheath. In contrast to their normal TTX sensitivity, the voltage dependent Na currents recorded from these all glial nerves are insensitive to TTX (5 μM) but disappear when the external Na is replaced by TMA. The results suggest that in situ glial voltage dependent membrane properties depend on interactions between the glial cells and the neighboring axons. © 1993 Wiley‐Liss, Inc.
Glial plasmalemmal vesicles: A subcellular fraction from rat hippocampal homogenate distinct from synaptosomes
Authors: Nakamura Yoichi , Iga Kozo , Shibata Taiho , Shudo Masachika , Kataoka Kiyoshi 
Published: January 2005

AbstractBy a Percoll density‐gradient centrifugation of rat hippocampal ho‐mogenate, We found a novel subcellular fraction (specific gravity ≈ 1.046 g/ml), besides synaptosomes (≈1.060 g/ml), which showed a high activity of Na+‐dependent glutamate uptake. The initial rate of the glutamate uptake in this fraction was as high as twice that in synaptosomes. Activities of choline acetyltransferase and high affinity choline uptake were, on the other hand, much lower. γ‐Aminobutyric acid uptake activity was nearly equivalent in both fractions. Electron microscopic observations revealed that the fraction was morphologically different from synaptosomal or myelin fractions, but mainly consisted of two different types of empty membrane vesicles; irregular (0.3−0.8 μm in diameter) and spheroid type (0.2 μm). The immunoreactivity to glial fibrillary acidic protein was appreciably high in this fraction. The marker enzyme analysis showed the fraction was rich in plasma membranes. On the basis of these results, the fraction is termed glial plasmalemmal vesicles(GPV).We analyzed kinetically the reaction of Na+ ‐dependent glutamate uptake by GPV comparing with that by synaptosomes. Km values for glutamate in GPV was 4.7 μM and Vmax was 33 nmol/mg/min, while in synaptosomes 11 μM and 17 nmol/mg/min, respectively. Hill coefficients of Na+ activation in GPV and synaptosome were 1.1 and 2.0, respectively. Thus, the mechanism or transporter molecule in glial cells for Na+‐dependent glutamate transport is likely to be different from that in neurons. © 1993 Wiley‐Liss, Inc.
Glutamate blocks astroglial stellation: Effect of glutamate uptake and volume changes
Authors: Shao Yanping , Enkvist M. O. Kristian , McCarthy Ken D. 
Published: January 2005

AbstractNeurotransmitters which increase intracellular cAMP levels can cause cultured astroglia to change from a flat, polygonal shape to a stellate morphology. Little is known about how glial stellation can be regulated by other transmitters. In the present study, we demonstrated that L‐glutamate blocked isoproterenol (ISO) or dibutyryl‐cAMP induced stellation in astroglia. The glutamate inhibition was concentration dependent, with its maximal effect on >90% of cells at 500 μM. Glutamate also reversed glial stellation within a short period (<30 min). Glutamate uptake analogues, D‐glutamate and D‐aspartate, rather than receptor agonists, kainate and quisqualate, mimicked the glutamate effect. Likewise, the glutamate uptake blocker, D‐thero‐ß‐hydroxyaspartate, blocked the glutamate effect. The glutamate inhibition was not a result of inhibition of cAMP formation, since norepinephrine, which inhibited 80% of ISO‐stimulated cAMP, also caused glial stellation. Increases in extracellular K+ to 50 mM also reduced glial stellation, whereas 25 mM K+ had little effect. Since 25 mM K+ caused much greater depolarization than 400 μM glutamate, it was unlikely that the effects of both glutamate and high [K+] on glial stellation were due to membrane depolarization. Hypotonic treatment (120 mOsm) enhanced, whereas hypertonic treatment (520 mOsm) prevented, the glutamate reversal of glial stellation. Thus, glial swelling appeared to be a primary mechanism for the inhibitory effect of glutamate and high [K+] on glial stellation. This mechanism could also explain the observation that glutamate inhibited stellation induced by PMA, a PKC activator. Our data suggest that glutamate released from neurons during neuronal activity or pathology can be taken up by astrocytes and alter their morphology. Changes in glial morphology may in turn affect the volume and composition of the extracellular space and, as a result, neuronal activity. © 1994 Wiley‐Liss, Inc.
Development of microglia in mouse neopallial cell cultures
Authors: Neuhaus Jochen , Fedoroff Sergey 
Published: January 2005

AbstractMicroglia develop in cultures initiated from disaggregated neopallial cells of newborn C3H/HeJ mice when the cultures are subjected to nutritional deprivation for 10 or more days (Hao et al: Int J Dev Neurosci 9:1‐14, 1991). In the present experiments, the cultures were pulsed with BrdU for 3 hours at different times during incubation and then the cells were immunoreacted with antibodies against BrdU, GFAP, and CR3 receptor. The dividing cells (BrdU+) were found to be either GFAP+ or GFAP−, but not Mac‐1+/BrdU+. Infection of proliferating cells after 2 or more days of incubation with replication‐deficient retroviral vector containing E. coli lacZ reporter gene resulted in many labeled astroglia cell clones but no labeled microglia. However, when cells were infected right after disaggregation of neopallium, labeled Mac‐1+ microglia were found. When Mac‐1+ cells in a suspension of disaggregated neopallial cells were killed using complement mediated lysis before setting up the cultures, Mac‐1+ microglia developed, in spite of the treatment. We conclude that in cultures initiated from mouse neopallium there are MAC‐1−/GFAP− microglia progenitor cells which do not divide in nutritionally deprived cultures but can transform into Mac‐1+ microglia under the influence of astroglia‐derived trophic factors. Microglia, which become Mac‐1+ (i.e., express CR3 receptor), proliferate extensively in the presence of CSF‐1 (which is produced by astroglia). © 1994 Wiley‐Liss, Inc.
Divergent lineages for oligodendrocytes and astrocytes originating in the neonatal forebrain subventricular zone
Authors: Luskin Marla B. , McDermott Kieran 
Published: January 2005

AbstractAlthough previous studies have revealed that the prenatal rat ventricular zone contains separate progenitor cells for neurons, astrocytes, and oligodendrocytes during the development of the cerebral cortex as early as the beginning of neurogenesis (Luskin et at., 1993; Grove et al., 1993), it is still unclear whether there are bipotential progenitor cells in the neonatal telencephalic subventricular zone which give rise to both astrocytes and oligodendrocytes during the peak of gliogenesis. To investigate this possibility, discrete groups of clonally related cells, generated by infecting progenitor cells of the neonatal subventricular zone with a retroviral lineage tracer, were analyzed ultrastructurally.An intracerebral injection of retrovirus encoding the reporter gene E. coli ß‐galactosidase (lacZ) was made into the subventricular zone of newborn rats. Two weeks later their brains were perfused, sectioned, and histochemically reacted with X‐Gal to identify at the light microscopic level clones of lacZ‐positive cells. The sections were processed for electron microscopy to enable the identity of clonally related cells to be assessed at the ultrastructural level.All of the clones analyzed contained cells of the same phenotype and could be divided into four distinct types: immature cell clones situated in the subependymal zone surrounding the lateral ventricle, oligodendrocytes clones, and white or gray matter astrocyte clones. Not all of the cells in every clone displayed ultrastructural features of a mature cell. Rather, in some glial clones the lacZ‐positive cells appeared to be at different stages of differentiation. However, we never encountered clones which contained both macroglial subtypes or clones containing neurons. Although the existence of bipotential progenitor cells cannot be completely dismissed, our results indicate the absence of progenitor cells in vivo in the neonatal subventricular zone which divide and generate astrocytes and oligodendrocytes. © 1994 Wiley‐Liss, Inc.
Transport of L‐arginine in cultured glial cells
Authors: Schmidlin Andreas , Wiesinger Heinrich 
Published: January 2005

AbstractUptake of radiolabelled L‐arginine was studied in four different kinds of glial cultures, in astroglia‐rich primary cultures derived from neonatal rat and mouse brains, in pure murine astrocyte cultures, and in rat glioma cells C6‐BU‐1. A saturable component of uptake was found in all cases with KM values between 15 and 35 μM and Vmax values between 0.8 and 2.5 nmol · min−1 · (mg protein)−1. In addition, in all cell types a non‐saturable component dominated total uptake at high concentrations of extracellular arginine. Rates of uptake of arginine were not affected when Na+ or Cl− were absent from the incubation buffer. Carrier‐mediated uptake of arginine was reduced by depolarizing concentrations of K+ and strongly inhibited by an excess of lysine or ornithine. Histidine, asparagine, glutamine, citrulline, creatine, NG‐nitro‐L‐arginine, NG‐monomethyl‐L‐arginine, or L‐canavanine inhibited L‐arginine transport to various degrees. Uptake of arginine was not reduced in the presence of serine or alanine, cysteic acid, N‐methyl‐α‐aminoisobutyric acid, or 2‐aminobicyclo‐(2.2.1)‐heptane‐2‐carboxylic acid. Rates of uptake of arginine were increased when cells had been preloaded with lysine. Preincubation of primary cultures, but not glioma cells, with bacterial lipopolysaccharide stimulated transport of arginine by increasing the Vmax value of uptake. This stimulation was dependent on protein synthesis. The results suggest that, at physiological concentrations, arginine is taken up into the glial cells with the help of the transport system “y+” for basic amino acids. In glial primary cultures, uptake of arginine appears to be regulated by compounds which also exert influence on nitric oxide synthesis. © 1994 Wiley‐Liss, Inc.
Stability over one year in patients admitted to a nursing home dementia unit
Authors: Rovner Barry W. , Lucas‐Blaustein Jane , Folstein Marshal F. , Smith Shannon W. 
Published: January 2005

AbstractThe majority of nursing home patients in the United States have dementia or behavioral problems yet the outcome of care they receive for those disorders is unknown. We compared the outcomes of Alzheimer's disease patients residing on a dementia unit with other Alzheimer's patients in the same nursing home over a one‐year period. We found that the functional capacity of dementia unit patients remained stable over the study period while that of non‐unit patients declined. This study suggests the usefulness of dementia units in nursing homes and raises issues relevant to their future study.
Single photon emission tomography in dementia
Authors: Beats Barbara , Burns Alistair , Levy Raymond 
Published: January 2005

AbstractSingle photon emission tomography (SPET) is a technique which allows simple non‐invasive measures of cerebral blood flow and indirectlymetabolism. It has considerablepotential as a tool for the differential diagnosis ofdementia. A review is presented tracing the development and current applications of the technique and the practical implications of its use.
The kingston standardized cognitive assessment
Authors: Rodenburg Martin , Hopkins Robert W. , Hamilton Pamela F. , Ginsburg Lynne , Nashed Yousery , Minde Nina 
Published: January 2005

AbstractIn spite of the fact that demographic trends show an increase in the number of elderly persons, and hence more diagnosed as suffering from senile dementia, the cognitive assessment of the organically brain damaged elderly person still too often depends on the use of brief and incomplete rating scales, and is thus often poorly performed. The simple dementia rating scales in current use may fail to provide the range or depth needed for an adequate evaluation of the individual patient. The Kingston Standardized Cognitive Assessment is offered as an improved method of assessment. This instrument is described here in terms of its structure, function, statistical properties and normative data. We also provide examples of its clinical use.
Clinical assessment of psychopathology among elderly residents (CAPER): Development and pilot testing of a screening instrument to detect the presence of psychiatric disorders among residents of long‐term instituions
Authors: Reichenfeld H. F. , Bazile E. , Khan B. B. , Raman S. 
Published: January 2005

AbstractAlthough psychiatric illnesses are common occurrences in institutions taking care of the elderly, admission is seldom preceded by a mental health evaluation and only rarely are there provisions for ongoing psychiatric care. Screening a population for specific psychiatric disorders is traditionally carried out by lay interviewers. In field studies organized under the Epidemiological Catchment Area Program of the National Institute of Mental Health they were specially trained to complete the Diagnostic Interview Schedule (DIS) (Munson et al., 1985; Robins et al., 1985). An initial examination carried out by a trained psychiatrist can, however, also be regarded as a screen for the detection of the presence or absence of a psychiatric disorder, and defining a ‘case’ (Leighton et al., 1966). It represents the first step in the evaluation. The establishment of a specific diagnostic label, though at times possible as a result of one examination, is more usually determined at the second, third or fourth step after obtaining additional information from relatives or caregivers, and assessing the results of neuropsychological and biological tests. CAPER (Clinical Assessment of Psychopathology among Elderly Residents) was developed to provide in a semistructured format such a typical initial examination of elderly residents of long‐term institutions. It is designed to represent the first step in a comprehensive evaluation, can be completed in 15–20 minutes and generates clinically useful information. CAPER allows the examiner to draw conclusions commonly encountered in everyday practice and gives a choice between (1) no psychopathology, (2) definite psychopathology and (3) suspected psychopathology. A great deal of demographic data are also accumulated and entered into a specifically designed multi purpose computer program. The program can be used for epidemiological studies to determine the prevalence of specific disorders in different populations, but also has applications in correlating the findings of an initial clinical examination with the results of neuropsychological tests.
Does visuospatial memory in senile dementia of the Alzheimer type depend on the severity of the disorder?
Authors: Sahgal Arjun , Lloyd Stephen , Wray Catherine J. , Galloway Peter H. , Robbins Trevor W. , Sahakian Barbara J. , McKeith Ian G. , Cook Julia H. , Disley Jennifer C. A. , Edwardson James A. 
Published: January 2005

AbstractVisuospatial memory was studied in patients suffering from senile dementia of the Alzheimer type (SDAT). They had been allocated into one of two groups depending on the severity of their disorder (mild or moderate), and a control group of healthy elderly subjects was included. Three different microcomputer‐controlled tasks were used. The spatial span task was able to distinguish between the two SDAT groups. Both groups were impaired, relative to control, on spatial recognition. The deficit in spatial working memory was also equivalent in the mild and moderate groups and was accompanied by evidence of an intact strategic approach to the task. The normal positive relationship between spatial memory performance and strategy was in fact reversed in the SDAT groups, suggesting a pure spatial memory deficit. These results show that spatial memory processes are impaired in the early stages of SDAT and get worse as the disease progresses. They also suggest that the neuroanatomical foci of the deficits may be predominantly in posterior cortical regions (including hippocampus), rather than the frontal cortex.
Dementia of frontal lobe type in monozygotic twins
Authors: Hodgson R. E. , Barrett K. , Crook R. 
Published: January 2005

AbstractA pair of monozygotic twins who are concordant for dementia of frontal lobe type are discussed. This is believed to be the first case report of twins with this type of dementia. The salient features of dementia of frontal lobe type are also discussed.
Neural modeling and functional neuroimaging
Authors: Horwitz Barry , Sporns Olaf 
Published: January 2005

AbstractTwo research areas that so far have had little interaction with one another are functional neuroimaging and computational neuroscience. The application of computational models and techniques to the inherently rich data sets generated by “standard” neurophysiological methods has proven useful for interpreting these data sets and for providing predictions and hypotheses for further experiments. We suggest that both theory‐ and data‐driven computational modeling of neuronal systems can help to interpret data generated by functional neuroimaging methods, especially those used with human subjects. In this article, we point out four sets of questions, addressable by computational neuroscientists whose answere would be of value and interest to those who perform functional neuroimaging. The first set consist of determining the neurobiological substrate of the signals measured by functional neuroimaging. The second set concerns developing systems‐level models of functional neuroimaging data. The third set of questions involves integrating functional neuroimaging data across modalities, with a particular emphasis on relating electromagnetic with hemodynamic data. The last set asks how one can relate systems‐level models to those at the neuronal and neural ensemble levels. We feel that there are ample reasons to link functional neuroimaging and neural modeling, and that combining the results from the two disciplines will result in furthering our understanding of the central nervous system. © 1994 Wiley‐Liss, Inc.This Article is a US Goverment work and, as such, is in the public domain in the United State of America.
Neural network interactions related to auditory learning analyzed with structural equation modeling
Authors: Gonzalez‐Lima F. , McLntosh A. R. 
Published: January 2005

AbstractIf learning is an emergent property of interacting brain regions, understanding it requires a network analysis of the patterns of interaction between brain regions. Brain mapping techniques have the potential of providing information about functional interactions within entire neural systems, but computational methods are needed to make sense of the complex interactions that take place in the brain. This review paper illustrates, with examples from auditory learning studies, the application of a computational method that quantifies the interactions among neural regions in terms of networks, and what is gained from this approach. The method is Structural Equation Modeling, and it computes network interactions by combining anatomical circuitry with the covariation in the activity between auditory structures. Activity was assessed by fluorodeoxyglucose uptake, and the functional strengths of auditory pathways were quantified by computing path coefficients representing the strength of the functional influence through each anatomical path. Changes in these values were used as indices of how learned information was processed and modified within the auditory system. Structural models of the auditory system revealed the patterns of network interactions related to habituation to a sound, as well as the patterns related to the opposite learned associative properties of the same sound. They illustrated how the functional interactions among parallel auditory neural pathways were modified as a result of auditory learning. This analysis supports the hypothesis that auditory learning is an emergent network property, distributed among connected brain regions showing specific patterns of interaction. ©1994 Wiley‐Liss, Inc.