bluuebunny/crossref_metadata_2025_split huggingface dataset:
Characterization of a novel oligodendrocyte cell surface molecule
Authors: Zhou L. , Szigeti V. , Miller R. H. 
Published: January 2005

AbstractCell‐type‐specific reagents have proven useful in the analysis of central nervous system (CNS) development and function. Most markers of oligodendrocytes are components of myelin sheath, which in the CNS is the specific product of oligodendrocytes. We have isolated a novel monoclonal antibody termed 2B10 which was raised against embryonic rat spinal cord tissue. In adult rat cerebrum, cerebellum, and spinal cord, 2B10 immunoreactivity is predominantly localized in white matter. 2B10 immunoreactivity is absent from peripheral nerve, suggesting that in the nervous system the 2B10 antigen is restricted to the CNS. Dissociated cell culture studies indicate that 2B10 labels a cell surface molecule, and its cellular distribution is coincident with O1 and myelin basic protein‐positive oligodendrocytes. By contrast, 2B10 does not label GFAP‐positive astrocytes. These data suggest that in the CNS the 2B10 antigen is expressed specifically on oligodendrocytes. Biochemical analysis indicates that 2B10 recognizes a protein with an apparent molecular weight of approximately 79,000 in reducing sodium dodecyl sulfate‐polyacrylamide gel electrophoresis. Developmentally, 2B10 immunoreactivity is detectable in rat spinal cord at as early as embryonic day 14. The relative abundance of this molecule decreases during myelination, but is maintained at a sustained level throughout adulthood. The 2B10 antigen appears not to be a myelin‐associated protein since it is not detected in purified myelin fractions. 2B10 immunoreactivity is not detectable in extracts of rat sciatic nerve, heart, kidney, muscle, and skin, but is detectable in extracts of spleen and thymus. These data suggest that the 2B10 antigen is a novel cell surface molecule that is expressed on oligodendrocyte lineage cells throughout development. © 1995 Wiley‐Liss, Inc.
Blockade of K+ channels induced by AMPA/kainate receptor activation in mouse oligodendrocyte precursor cells is mediated by NA+ entry
Authors: Borges K. , Kettenmann H. 
Published: January 2005

AbstractAMPA/kainate receptor activation in cultured oligodendrocyte precursor cells from embryonic mouse cortex leads to a blockade of delayed rectifying K+ currents. In the present study, we provide evidence using the patch‐clamp technique in the whole‐cell configuration that the mechanism linking kainate receptor activation and K+ conductance blockade is due to the receptor‐mediated Na+ entry: (1) The blockade was not observed in Na+ ‐free bathing solution nor when intracellular [Na+] was elevated by dialzying the cell with a pipette solution containing high [Na+]. (2) Elevation of intracellular [Na+] alone led to a blockade of outward currents in contrast to cells dialyzed by sucrose. High [Li+]i also reduced the outward currents, and in Li+‐containing bathing solution the kainate‐induced blockade of K+ channels was more pronounced. Probably, Li+ accumulates intracellularly after permeation through the receptor pore due to slower extrusion mechanisms. Experiments with GTPγS or GDPβS and pertussis toxin indicated that GTP‐binding protein‐mediated mechanisms were not of importance for the kainate‐induced K+ conductance blockade. Our data suggest that in glial precursor cells AMPA/kainate receptor activation leads to an intracellular [Na+] increase which blocks delayed rectifying K+ channels. © 1995 Wiley‐Liss, Inc.
Serum‐free B27/neurobasal medium supports differentiated growth of neurons from the striatum, substantia nigra, septum, cerebral cortex, cerebellum, and dentate gyrus
Authors: Brewer G. J. 
Published: January 2005

AbstractTwo fundamental questions about neuron cell culture were addressed. Can one serum‐free medium that was developed for optimum growth of hippocampal neurons support the growth of neurons from other regions of the brain? Is the region specific state of differentiation maintained in culture? To answer these questions, we isolated neurons from six other rat brain regions, placed them in culture in B27/NeurobasalTM defined medium, and analyzed their morphology and growth dependence on cell density after 4 days in culture. Neuronal identity was confirmed by immunostaining with antibodies to neurofilament 200. Neurons from each brain region maintained distinctive morphologies in culture in the virtual absence of glia. Cells isolated from embryonic day 18 cerebral cortex by digestion with papain showed the same high survival as hippocampal neurons, e.g., 70% survival for cells plated at 160/mm2. At this age and density, neurons from the septum showed slightly lower survival, 45%. Survival of dentate granule neurons from postnatal day four brains was 30‐40%, significantly lower, and relatively independent of plating density. This suggests an absence of dependence on trophic factors or contact for dentate granule neurons. Growth of cerebellar granule neurons isolated from postnatal day 7, 8, or 9 brains in B27/Neurobasal was compared to growth in BME/10% serum. Viability in serum‐free medium at 4 days was much better than that in serum, did not require KCI elevated to 25 mM, and occurred without substantial growth of glia. Cerebellar granule neurons plated at 1,280 cells/mm2 were maintained in culture for three weeks with 17 of the original cell density surviving. Survival of cells isolated from embryonic day 18 substantia nigra was 50% at 160 cells/mm2 after 4 days, similar to that of striatum, but slightly less than hippocampal neuron survival. The dopaminergic phenotype of the substantia nigral neurons was maintained over 2 weeks in culture as judged by immunoreactivity with antibodies to tyrosine hydroxylase. During this time, immunoreactivity was found in the processes as they grew out from the soma. Together, these studies suggest that B27/Neurobasal will be a useful medium for maintaining the differentiated growth of neurons from many brain regions. Potential applications of a common growth medium for different neurons are discussed. © 1995 Wiley‐Liss, Inc.
Increase in dopamine turnover and tyrosine hydroxylase enzyme in hippocampus of rats fed on low selenium diet
Authors: Castaño A. , Ayala A. , Rodriguez‐Gomez J. A. , De La Cruz C. P. , Revilla E. , Cano J. , Machado A. 
Published: January 2005

AbstractWe have studied the turnover of dopamine, noradrenaline, and serotonin and their metabolites in hippocampus of adult female rats that were fed control or selenium‐deficient diets during 15 days. Under these circumstances, there was an increase of dopamine turnover (4‐fold) in rats fed with selenium‐deficient diet with respect to controls and also an increase in the tyrosine hydroxylase activity (75.8%), which was the result of the increase of the amount of the enzyme (2‐fold), without significant change in the phosphorylation of the tyrosine hydroxylase.In addition the glutathione peroxidase, glutathione reductase, catalase, and superoxide dismutase activities have been studied. After selenium‐deficient diet, the enzymatic activities of superoxide dismutase and catalase did not show change with respect to the controls; however glutathione reductase and glutathione peroxidase significantly decreased 15% and 29%, respectively.It is concluded that the increase in dopamine turnover seems to be associated with the induction of tyrosine hydroxylase enzyme. In these conditions the decrease in antioxidant capacity may produce a cascade of events, which accelerates the degenerative process, since the increase in dopamine turnover produces an increase in oxygen radical by monoamine oxidase activity. © 1995 Wiley‐Liss, Inc.
Detection of tenascin‐C in the nervous system of the tenascin‐C mutant mouse
Authors: Mitrovic N. , Schachner M. 
Published: January 2005

AbstractWe have investigated the expression of tenascin‐C (TN‐C) in the somatosensory cortex of early postnatal mutant mice in which lacZ was reported to be expressed in place of tenascin (Saga et al.: Genes Dev 6:1821‐1831, 1992). At both the mRNA and protein levels, TN‐C was detected at levels lower in the mutant than in wild type animals by in situ hybridization and by immunocytochemistry using several poly‐ and monoclonal antibodies directed against mouse TN‐C. The distribution of TN‐C immunoreactivity in coronal sections was abnormal in that the barrel field boundaries in layer 4 of the somatosensory cortex could not be detected in the mutant mice. Furthermore, TN‐C was detected intracellularly in most cell bodies, including possibly also neurons. Western blot analysis of homogenates of brain tissue from early postnatal animals showed an abnormal pattern of protein bands immunoreactive for TN‐C in mutant animals while β‐galactosidase migrated at its expected molecular weight without incorporation into fusion proteins with TN‐C, suggesting disturbed splicing mechanisms. No gross disturbances in the patterning of barrel fields could be detected in the mutant mice as shown by Nissl staining. Our observations show that the mutant mouse designed to be nully disrupted for TN‐C expression shows detectable and abnormal TN‐C expression. © 1995 Wiley‐Liss, Inc.
Immunological identification of A1 adenosine receptors in brain cortex
Authors: Ciruela F. , Casadó V. , Mallol J. , Canela E. I. , Lluis C. , Franco R. 
Published: January 2005

AbstractThe A1 adenosine receptor from pig brain cortex has been identified by means of two antipeptide antibodies against two domains of the receptor molecule: PC/10 antiserum was raised against a part of the third intracellular loop, and PC/20 antiserum was raised against a part of the second extracellular loop. PC/10 antibody was able to recognize a 39‐kDa band that corresponded to the Al receptor, as demonstrated by immunoblotting and by immunoprecipitation of the molecule cross‐linked to [125I](R)‐2‐azidoN2‐p‐hydroxy(phenylisopropyl)adenosine. Besides the 39‐kDa band, PC/20 also recognized a 74‐kDa form that does not seem to correspond to a receptor‐G protein complex. The occurrence of the two bands was detected and analyzed in samples from different species and tissues showing a heterogeneous distribution of both. The 74‐kDa form can be converted into the 39‐kDa form by treatment with agonists or antagonists of Al adenosine receptors. These results suggest that A1 adenosine receptor can occur in dimers and that the dimer–monomer conversion might be regulated by adenosine as the physiological ligand. Since the 74‐kDa aggregates were not recognized by PC/10, it is likely that part of the third intracellular loop participates in the protein–protein interaction. ©1995 Wiley‐Liss, Inc.
Experimental allergic encephalomyelitis: Characterization of T lymphocytes that bind myelin basic protein and synapsin
Authors: de Santis M. L. , Roth G. A. 
Published: January 2005

AbstractThe immuno phenotypic profile of the mononuclear cells that bind myelin basic protein (MBP) and synapsin was investigated in lymph node cells from rats with experimental allergic encephalomyelitis induced by injection with MBP. Using a double immunofluorescent labeling technique, purified cells that bind one or both antigens were analyzed in different stages of the disease. The total MBP‐bound lymphocytes increased at 14 days post‐inoculation (dpi), had a CD4+/CD8+ ratio of two and were present until 29 dpi. Conversely, the apportionment of cells specific for MBP that also recognize synapsin reached a maximum value at 14 dpi coincidentally with the expression of the paralysis symptoms and then, they disappeared when the animal began to recover. This population amounted to about 40% of the total lymph node MBP‐bound cells and had a CD4+/CD8+ ratio of one, indicating that the lymphocytes with MBPsynapsin crossreactivity could be principally implicated in a cytotoxic or suppressor activity. © 1996 Wiley‐Liss, Inc.
Dietary β‐alanine results in taurine depletion and cerebellar damage in adult cats
Authors: Lu P. , Xu W. , Sturman J. A. 
Published: January 2005

AbstractWe have used the taurine analogue, β‐alanine, to perturb the taurine concentrations in taurine‐supplemented and taurine‐deprived adult cats. By using 5 % β‐alanine in the drinking water for 20 weeks, both groups of cats had greatly reduced brain taurine concentrations. Taurine‐supplemented cat brain accumulated relatively small amounts of β‐alanine whereas taurine‐deprived cats accumulated large amounts of β‐alanine. The cerebellum of cats treated with β‐alanine had a number of pathological changes compared with similar cats drinking water alone. The changes were more severe in the taurine‐deprived cats, and included reduced numbers of granule and Purkin je cells, with many of those remaining appearing pyknotic and dying. Long swollen fibers were seen in the white matter, resembling Rosenthal fibers described in some human cerebellar diseases. There was also prominent gliosis. Using antibodies to β‐alanine and taurine, β‐alanine was localized in Purkinje cell soma and dendrites, in Golgi II cells, and in some granule cells, especially in taurine‐deprived cats treated with β‐alanine. Taurine appears to have been virtually eliminated from Purkinje and granule cells, and concentrated in Golgi II cells and glia. We conclude that β‐alanine is responsible for these neuro toxic pathological changes. © 1996 Wiley‐Liss, Inc.
Nitrogen fertilizer and seed rate effects on Hagberg falling number of hybrid wheats and their parents are associated with α‐amylase activity, grain cavity size and dormancy
Authors: Kindred Daniel R , Gooding Mike J , Ellis Richard H 
Published: January 2005

AbstractField experiments were carried out to assess the effects of nitrogen fertilization and seed rate on the Hagberg falling number (HFN) of commercial wheat hybrids and their parents. Applying nitrogen (200 kg N ha−1) increased HFN in two successive years. The HFN of the hybrid Hyno Esta was lower than either of its parents (Estica and Audace), particularly when nitrogen was not applied. Treatment effects on HFN were negatively associated with α‐amylase activity. Phadebas grain blotting suggested two populations of grains with different types of α‐amylase activity: Estica appeared to have a high proportion of grains with low levels of late maturity endosperm α‐amylase activity (LMEA); Audace had a few grains showing high levels of germination amylase; and the hybrid, Hyno Esta, combined the sources from both parents to show heterosis for α‐amylase activity. Applying nitrogen reduced both apparent LMEA and germination amylase. The effects on LMEA were associated with the size and disruption of the grain cavity, which was greater in Hyno Esta and Estica and in zero‐nitrogen treatments. External grain morphology failed to explain much of the variation in LMEA and cavity size, but there was a close negative correlation between cavity size and protein content. Applying nitrogen increased post‐harvest dormancy of the grain. Dormancy was greatest in Estica and least in Audace. It is proposed that effects of seed rate, genotype and nitrogen fertilizer on HFN are mediated through factors affecting the size and disruption of the grain cavity and therefore LMEA, and through factors affecting dormancy and therefore germination amylase. Copyright © 2004 Society of Chemical Industry
Brain energy metabolism and dopaminergic function in Huntington's disease measured in vivo using positron emission tomography
Authors: Leenders K. L. , Frackowiak R. S. J. , Quinn N. , Marsden C. D. 
Published: January 2005

AbstractA 48‐year‐old man with typical Huntington's disease was investigated with computed tomography (CT) and positron emission tomography. Regional cerebral blood flow, oxygen extraction, oxygen and glucose utilisation, L‐Dopa uptake, and dopamine (D2) receptor binding were measured using several positron‐labelled tracers. CT showed slight atrophy of the head of caudate but no cortical atrophy, although distinct frontal lobe dysfunction was present on psychometric testing. Oxygen and glucose metabolism and cerebral blood flow were decreased in the striata and to a lesser extent in frontal cortex. Cerebral blood flow was in the low normal range throughout the remainder of the brain. A normal metabolic ration was found in all regions, since the changes in glucose utilisation paralleled those in oxygen consumption. The capacity of the striatum to store dopamine as assessed by L‐[18F]‐fluorodopa uptake was normal, but dopamine (D2) receptor binding was decreased when compared to normal subjects.
The effect of single and repeated administration of bromocriptine on monoamine metabolism in rat brain and [3H]spiroperidol binding to striatal membranes
Authors: Muradas V. , Bazan E. , Gervas J. J. , Mena M. A. , de Yebenes J. G. 
Published: January 2005

AbstractAdministration of a single high dose of bromocriptine decreased synthesis and release of dopamine and serotonin in several brain regions, most notably in the striatum. Bromocriptine modified the kinetics of [3H]spiroperidol binding to striatal membranes, but these changes were not prominent 2 h after injection when modifications of monoamine metabolism were evaluated. After injection of the same dose of bromocriptine daily for 10 days, the decrease in dopamine synthesis persisted, while other aspects of monoamine metabolism, presumably controlled by dopamine autoreceptors, returned to normal values. This adaptation was not caused by decreased blood levels of bromocriptine, since bromocriptine accumulated in plasma after repeated drug administration. This study provides evidence that different aspects of dopamine cell function, presumably controlled by autoreceptors, show different patterns of adaptation after chronic administration of dopamine agonists.
Long‐term followup computed tomography and magnetic resonance imaging findings in hepatolenticular degeneration: Case report and summary of the literature
Authors: Metzer W. Steven , Angtuaco Edgardo 
Published: January 2005

AbstractPretreatment and long‐term followup computed tomography (CT) findings were reported in a patient with successfully treated Wilson's disease. Results of magnetic resonance imaging (MRI) are correlated with followup CT findings, with MRI being more specifically sensitive than CT. The literature of CT and MRI findings in Wilson's disease is reviewed and summarized.
Natural history and treatment of tardive dystonia
Authors: Kang Un Jung , Burke Robert E. , Fahn Stanley 
Published: January 2005

AbstractWe retrospectively reviewed the clinical course and response to treatment of 67 patients with tardive dystonia. The age at onset ranged from 13 to 72 years without predilection to any particular age group or sex. Patients developed tardive dystonia even after relatively short duration of exposure to dopamine antagonists (21% within one year). Five of 42 patients withdrawn from these drugs remitted. Overall clinical improvement occurred in 52% of patients. Tetrabenazine and reserpine were most effective (>50% response rate) in controlling dystonia. Anticholinergic drugs diminished dystonia in 46% of patients.
Essential tongue tremor
Authors: Biary Nabil , Koller William C. 
Published: January 2005

AbstractTwenty patients with tongue tremor associated with essential tremor are reported. Patients were unaware of the tongue tremor, and voice disturbance was a complaint in only one patient. Three patients had an isolated tongue tremor. Hand tremor was present in 16 patients. Dystonia, myoclonus, and tremor of other body parts were present in some patients. Three patients had a mild‐to‐moderate dysarthria. The frequency of tongue tremor (4–8 Hz) was identical to hand tremor. The intravenous infusion of ethanol suppressed tongue tremor. Therapy with propranolol, primidone, or clonazepam also reduced tongue tremor amplitude. Tongue tremor is a common finding in some essential tremor patients but often there are no symptoms.
Young onset Parkinson's disease
Authors: Quinn Niall , Critchley Peter , Marsden C. David 
Published: January 2005

AbstractWe describe a personal series of 60 cases of parkinsonism with onset under the age of 40 years. Known causes for early onset of secondary parkinsonism, such as Wilson's disease or encephalitis, were excluded in every case. Two groups were identified: those with onset after the age of 21 in whom no hereditary factors could be ascertained (56 cases), and those with onset before 21 years all of whom had familial parkinsonism. In neither group have we found any association with prematurely grey hair, hypertension, diabetes, pernicious anaemia, or thyroid disorder. Among their families, we have not found any association with diabetes, pernicious anaemia, or thyroid disorder. We propose that cases of apparent idiopathic Parkinson's disease begining between age 21–40 years should be called “young onset Parkinson's disease.” Twenty percent of such patients in our series had at least one first‐ or second‐degree relative in the same or antecedent generations with parkinsonism, but only 1.5% of their relatives at risk had parkinsonism, which is similar to the prevalence in the general population. Ten percent of these patients had at least one relative with essential tremor, but only 1.6% of their relatives at risk had tremor, which again was similar to the prevalence in the population in general. These patients with young onset Parkinson's disease responded well to levodopa therapy. However, dyskinesias and response fluctuations occurred early and frequently. The prevalence of dyskinesias and response fluctuations was strongly correlated with the duration of levodopa treatment, but not with the duration (or probably the severity) of the disease before levodopa therapy was commenced. The involuntary movements often were severe and frequently were diphasic. Despite long disease duration, the incidence of dementia in young onset patients aged less than 65 years was negligible. We believe that most, if not all, patients in this group have degenerative Lewy body idiopathic Parkinson's disease, representing the lower end of a skewed deviation for age of onset of this disease. We have so far failed to identify any additional environmental factor which may have accelerated disease onset in these patients. In contrast, cases of parkinsonism beginning before age 21 years were invariably familial. We proposed that they should be called “juvenile parkinsonism.” All affected relatives with parkinsonism also had young disease onset, and all but one were siblings. None of four such patients seen by us has demented, and computed tomography (CT) scan has been normal in all four. We believe that most such patients have some form of genetically determined secondary parkinsonism.
A new syndrome of axial muscle rigidity associated with etretinate therapy
Authors: Albin Roger L. , Silverman Alan K. , Ellis Charles N. , Voorhees John J. , Albers James W. 
Published: January 2005

AbstractWe report on three cases of a novel syndrome associated with treatment for psoriasis with the retinoid etretinate. The distinctive features of this syndrome include rigidity that is restricted to the axial muscles, impairment of neck extension greater than flexion, impairment of anteflexion at the waist, severe impairment of lateral flexion at both the waist and the neck, and, in one case, rigidity of proximal lower extremity muscles. Peripheral nerve block extinguished the lower extremity rigidity in one patient, and two patients had a favorable response to Sinemet. One patient had persistence of symptoms and findings 2 years after discontinuation of etretinate. The clinical features of this syndrome are consistent with an effect of etretinate on central, possible catecholaminergic neurons.