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  • 1
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    Induction of nitric oxide-dependent apoptosis in motor neurons by zinc-deficient superoxide dismutase (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-01-05
    Description: Mutations in copper, zinc superoxide dismutase (SOD) have been implicated in the selective death of motor neurons in 2 percent of amyotrophic lateral sclerosis (ALS) patients. The loss of zinc from either wild-type or ALS-mutant SODs was sufficient to induce apoptosis in cultured motor neurons. Toxicity required that copper be bound to SOD and depended on endogenous production of nitric oxide. When replete with zinc, neither ALS-mutant nor wild-type copper, zinc SODs were toxic, and both protected motor neurons from trophic factor withdrawal. Thus, zinc-deficient SOD may participate in both sporadic and familial ALS by an oxidative mechanism involving nitric oxide.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Estevez, A G -- Crow, J P -- Sampson, J B -- Reiter, C -- Zhuang, Y -- Richardson, G J -- Tarpey, M M -- Barbeito, L -- Beckman, J S -- R01 HL58209/HL/NHLBI NIH HHS/ -- R01 NS33291/NS/NINDS NIH HHS/ -- R01 NS36761/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1999 Dec 24;286(5449):2498-500.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anesthesiology, University of Alabama at Birmingham, Birmingham, AL 35233, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10617463" target="_blank"〉PubMed〈/a〉
    Keywords: Amyotrophic Lateral Sclerosis/drug therapy/*enzymology/genetics/pathology ; Animals ; *Apoptosis ; Brain-Derived Neurotrophic Factor/pharmacology ; Cells, Cultured ; Chelating Agents/pharmacology ; Copper/metabolism ; Fluoresceins/metabolism ; Liposomes ; Motor Neurons/*cytology/metabolism ; Mutation ; Nitrates/metabolism ; Nitric Oxide/*metabolism ; Nitric Oxide Synthase/antagonists & inhibitors/metabolism ; Nitric Oxide Synthase Type I ; Oxidation-Reduction ; Rats ; Superoxide Dismutase/chemistry/genetics/*metabolism/toxicity ; Superoxides/metabolism ; Zinc/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
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    Down-regulation of the macrophage lineage through interaction with OX2 (CD200) (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-12-02
    Description: OX2 (CD200) is a broadly expressed membrane glycoprotein, shown here to be important for regulation of the macrophage lineage. In mice lacking CD200, macrophage lineage cells, including brain microglia, exhibited an activated phenotype and were more numerous. Upon facial nerve transection, damaged CD200-deficient neurons elicited an accelerated microglial response. Lack of CD200 resulted in a more rapid onset of experimental autoimmune encephalomyelitis (EAE). Outside the brain, disruption of CD200-CD200 receptor interaction precipitated susceptibility to collagen-induced arthritis (CIA) in mice normally resistant to this disease. Thus, in diverse tissues OX2 delivers an inhibitory signal for the macrophage lineage.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hoek, R M -- Ruuls, S R -- Murphy, C A -- Wright, G J -- Goddard, R -- Zurawski, S M -- Blom, B -- Homola, M E -- Streit, W J -- Brown, M H -- Barclay, A N -- Sedgwick, J D -- New York, N.Y. -- Science. 2000 Dec 1;290(5497):1768-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉DNAX Research Institute of Molecular and Cellular Biology, 901 California Avenue, Palo Alto, CA 94304, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11099416" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD ; Antigens, Surface/*metabolism ; Arthritis, Experimental/immunology/pathology ; Cell Lineage ; Central Nervous System/immunology/pathology ; Denervation ; *Down-Regulation ; Encephalomyelitis, Autoimmune, Experimental/immunology/pathology ; Facial Nerve ; Gene Targeting ; Joints/immunology/pathology ; Lymph Nodes/cytology ; Macrophage Activation ; Macrophages/cytology/metabolism/*physiology ; Mice ; Mice, Inbred C57BL ; Microglia/physiology ; Neurons/physiology ; Rats ; Receptors, Immunologic/metabolism ; Spleen/cytology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    Differential shunting of EPSPs by action potentials (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-01-06
    Description: Neurons encode information and communicate via action potentials, which are generated following the summation of synaptic events. It is commonly assumed that action potentials reset the membrane potential completely, allowing another round of synaptic integration to begin. We show here that the conductances underlying the action potential act instead as a variable reset of synaptic integration. The strength of this reset is cell type-specific and depends on the kinetics, location, and timing of the synaptic input. As a consequence, distal synapses, as well as inputs mediated by N-methyl-d-aspartate receptor activation, can contribute disproportionately to synaptic integration during action potential firing.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hausser, M -- Major, G -- Stuart, G J -- New York, N.Y. -- Science. 2001 Jan 5;291(5501):138-41.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, University College London, Gower Street, London WC1E 6BT, UK. m.hausser@ucl.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11141567" target="_blank"〉PubMed〈/a〉
    Keywords: *Action Potentials/drug effects ; Animals ; Computer Simulation ; Dendrites/drug effects/physiology ; Electric Stimulation ; *Excitatory Postsynaptic Potentials/drug effects ; Kinetics ; Magnesium/pharmacology ; Models, Neurological ; Neocortex/cytology/physiology ; Patch-Clamp Techniques ; Purkinje Cells/*physiology ; Pyramidal Cells/*physiology ; Rats ; Receptors, AMPA/physiology ; Receptors, N-Methyl-D-Aspartate/physiology ; Synapses/physiology ; *Synaptic Transmission ; Tetrodotoxin/pharmacology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    Dependence of EPSP efficacy on synapse location in neocortical pyramidal neurons (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-03-09
    Description: Neurons receive thousands of synaptic inputs throughout elaborate dendritic trees. Here we determine the somatic impact of excitatory postsynaptic potentials (EPSPs) generated at known dendritic sites in neocortical pyramidal neurons. As inputs became more distal, somatic EPSP amplitude decreased, whereas use-dependent depression increased. Despite marked attenuation (〉40-fold), when coactivated within a narrow time window (approximately 10 milliseconds), distal EPSPs could directly influence action potential output following dendritic spike generation. These findings reveal that distal EPSPs are ineffective sources of background somatic excitation, but through coincidence detection have a powerful transient signaling role.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Williams, Stephen R -- Stuart, Greg J -- New York, N.Y. -- Science. 2002 Mar 8;295(5561):1907-10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Neuroscience, John Curtin School of Medical Research, Australian National University, Canberra, ACT 0200, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11884759" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Axons/physiology ; Dendrites/*physiology ; *Excitatory Postsynaptic Potentials ; Neocortex/cytology/*physiology ; Patch-Clamp Techniques ; Pyramidal Cells/*physiology ; Rats ; Rats, Wistar ; Synapses/*physiology ; Synaptic Transmission
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    Mutations in the DJ-1 gene associated with autosomal recessive early-onset parkinsonism (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-11-26
    Description: The DJ-1 gene encodes a ubiquitous, highly conserved protein. Here, we show that DJ-1 mutations are associated with PARK7, a monogenic form of human parkinsonism. The function of the DJ-1 protein remains unknown, but evidence suggests its involvement in the oxidative stress response. Our findings indicate that loss of DJ-1 function leads to neurodegeneration. Elucidating the physiological role of DJ-1 protein may promote understanding of the mechanisms of brain neuronal maintenance and pathogenesis of Parkinson's disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bonifati, Vincenzo -- Rizzu, Patrizia -- van Baren, Marijke J -- Schaap, Onno -- Breedveld, Guido J -- Krieger, Elmar -- Dekker, Marieke C J -- Squitieri, Ferdinando -- Ibanez, Pablo -- Joosse, Marijke -- van Dongen, Jeroen W -- Vanacore, Nicola -- van Swieten, John C -- Brice, Alexis -- Meco, Giuseppe -- van Duijn, Cornelia M -- Oostra, Ben A -- Heutink, Peter -- New York, N.Y. -- Science. 2003 Jan 10;299(5604):256-9. Epub 2002 Nov 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Genetic-Epidemiologic Unit, Department of Clinical Genetics, Department of Epidemiology and Biostatistics, Erasmus Medical Center Rotterdam, Post Office Box 1738, 3000 DR Rotterdam, Netherlands. bonifati@kgen.fgg.eur.nl〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12446870" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Amino Acid Sequence ; Amino Acid Substitution ; Animals ; Base Sequence ; Brain/metabolism ; COS Cells ; Cell Nucleus/metabolism ; Chromosomes, Human, Pair 1 ; Cloning, Molecular ; Cytoplasm/metabolism ; DNA, Complementary ; Exons ; Genes, Recessive ; Humans ; Intracellular Signaling Peptides and Proteins ; Molecular Sequence Data ; *Mutation ; Oncogene Proteins/chemistry/*genetics/metabolism ; Oxidative Stress ; PC12 Cells ; Parkinsonian Disorders/*genetics/metabolism ; Pedigree ; Physical Chromosome Mapping ; Point Mutation ; Protein Structure, Secondary ; Rats ; Reverse Transcriptase Polymerase Chain Reaction ; Sequence Deletion ; Transfection
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    Alteration of lymphocyte trafficking by sphingosine-1-phosphate receptor agonists (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-03-30
    Description: Blood lymphocyte numbers, essential for the development of efficient immune responses, are maintained by recirculation through secondary lymphoid organs. We show that lymphocyte trafficking is altered by the lysophospholipid sphingosine-1-phosphate (S1P) and by a phosphoryl metabolite of the immunosuppressive agent FTY720. Both species were high-affinity agonists of at least four of the five S1P receptors. These agonists produce lymphopenia in blood and thoracic duct lymph by sequestration of lymphocytes in lymph nodes, but not spleen. S1P receptor agonists induced emptying of lymphoid sinuses by retention of lymphocytes on the abluminal side of sinus-lining endothelium and inhibition of egress into lymph. Inhibition of lymphocyte recirculation by activation of S1P receptors may result in therapeutically useful immunosuppression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mandala, Suzanne -- Hajdu, Richard -- Bergstrom, James -- Quackenbush, Elizabeth -- Xie, Jenny -- Milligan, James -- Thornton, Rosemary -- Shei, Gan-Ju -- Card, Deborah -- Keohane, CarolAnn -- Rosenbach, Mark -- Hale, Jeffrey -- Lynch, Christopher L -- Rupprecht, Kathleen -- Parsons, William -- Rosen, Hugh -- New York, N.Y. -- Science. 2002 Apr 12;296(5566):346-9. Epub 2002 Mar 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology and Rheumatology, Merck Research Laboratories, Post Office Box 2000, Rahway, NJ 07065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11923495" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/drug effects/*physiology ; Binding, Competitive ; CHO Cells ; Calcium/metabolism ; Cricetinae ; Cyclic AMP/metabolism ; Fingolimod Hydrochloride ; Guanosine 5'-O-(3-Thiotriphosphate)/metabolism ; Humans ; Immunosuppressive Agents/metabolism/pharmacology ; Ligands ; Lymph Nodes/cytology/drug effects ; Lymphocyte Count ; Lymphopenia/chemically induced ; *Lysophospholipids ; Mice ; Organophosphates/chemical synthesis/chemistry/metabolism/*pharmacology ; Organophosphonates/chemical synthesis/chemistry/metabolism/*pharmacology ; Phosphorylation ; Propylene Glycols/*metabolism/pharmacology ; Rats ; Receptors, Cell Surface/*agonists/metabolism ; *Receptors, G-Protein-Coupled ; Receptors, Lysophospholipid ; Sphingosine/*analogs & derivatives/metabolism/*pharmacology ; Spleen/cytology/drug effects ; Stereoisomerism ; T-Lymphocytes/drug effects/*physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
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    Calcium sensitivity of glutamate release in a calyx-type terminal (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-08-11
    Description: Synaptic efficacy critically depends on the presynaptic intracellular calcium concentration ([Ca2+]i). We measured the calcium sensitivity of glutamate release in a rat auditory brainstem synapse by laser photolysis of caged calcium. A rise in [Ca2+]i to 1 micromolar readily evoked release. An increase to 〉30 micromolar depleted the releasable vesicle pool in 〈0.5 millisecond. A comparison with action potential-evoked release suggested that a brief increase of [Ca2+]i to approximately 10 micromolar would be sufficient to reproduce the physiological release pattern. Thus, the calcium sensitivity of release at this synapse is high, and the distinction between phasic and delayed release is less pronounced than previously thought.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bollmann, J H -- Sakmann, B -- Borst, J G -- New York, N.Y. -- Science. 2000 Aug 11;289(5481):953-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max-Planck-Institute for Medical Research, Department of Cell Physiology, Jahnstrasse 29, D-69120 Heidelberg, Germany. jbollman@mpimf-heidelberg.mpg.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10937999" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Brain Stem/*metabolism ; Calcium/*metabolism ; Excitatory Postsynaptic Potentials ; Glutamic Acid/*metabolism ; Patch-Clamp Techniques ; Photolysis ; Presynaptic Terminals/metabolism ; Rats ; Rats, Wistar ; Synapses/*metabolism ; Synaptic Transmission ; Synaptic Vesicles/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
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    Recycling endosomes supply AMPA receptors for LTP (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-09-28
    Description: Long-term potentiation (LTP) of synaptic strength, the most established cellular model of information storage in the brain, is expressed by an increase in the number of postsynaptic AMPA receptors. However, the source of AMPA receptors mobilized during LTP is unknown. We report that AMPA receptors are transported from recycling endosomes to the plasma membrane for LTP. Stimuli that triggered LTP promoted not only AMPA receptor insertion but also generalized recycling of cargo and membrane from endocytic compartments. Thus, recycling endosomes supply AMPA receptors for LTP and provide a mechanistic link between synaptic potentiation and membrane remodeling during synapse modification.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Park, Mikyoung -- Penick, Esther C -- Edwards, Jeffrey G -- Kauer, Julie A -- Ehlers, Michael D -- DA11289/DA/NIDA NIH HHS/ -- MH64748/MH/NIMH NIH HHS/ -- NS39402/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2004 Sep 24;305(5692):1972-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Duke University Medical Center, Box 3209, Durham, NC 27710, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15448273" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carrier Proteins/genetics/metabolism ; Cell Membrane/metabolism ; Cells, Cultured ; Endosomes/*metabolism ; Hippocampus/cytology ; *Long-Term Potentiation ; Neurons/metabolism ; Patch-Clamp Techniques ; Protein Transport ; Rats ; Rats, Sprague-Dawley ; Receptors, AMPA/*metabolism ; Synapses ; Transfection ; rab GTP-Binding Proteins/genetics/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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