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  • Neurons/*physiology  (2)
  • American Association for the Advancement of Science (AAAS)  (2)
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  • American Association for the Advancement of Science (AAAS)  (2)
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  • 1
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    dSarm/Sarm1 is required for activation of an injury-induced axon death pathway (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-06-09
    Description: Axonal and synaptic degeneration is a hallmark of peripheral neuropathy, brain injury, and neurodegenerative disease. Axonal degeneration has been proposed to be mediated by an active autodestruction program, akin to apoptotic cell death; however, loss-of-function mutations capable of potently blocking axon self-destruction have not been described. Here, we show that loss of the Drosophila Toll receptor adaptor dSarm (sterile alpha/Armadillo/Toll-Interleukin receptor homology domain protein) cell-autonomously suppresses Wallerian degeneration for weeks after axotomy. Severed mouse Sarm1 null axons exhibit remarkable long-term survival both in vivo and in vitro, indicating that Sarm1 prodegenerative signaling is conserved in mammals. Our results provide direct evidence that axons actively promote their own destruction after injury and identify dSarm/Sarm1 as a member of an ancient axon death signaling pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Osterloh, Jeannette M -- Yang, Jing -- Rooney, Timothy M -- Fox, A Nicole -- Adalbert, Robert -- Powell, Eric H -- Sheehan, Amy E -- Avery, Michelle A -- Hackett, Rachel -- Logan, Mary A -- MacDonald, Jennifer M -- Ziegenfuss, Jennifer S -- Milde, Stefan -- Hou, Ying-Ju -- Nathan, Carl -- Ding, Aihao -- Brown, Robert H Jr -- Conforti, Laura -- Coleman, Michael -- Tessier-Lavigne, Marc -- Zuchner, Stephan -- Freeman, Marc R -- 5R01-NS050557-05/NS/NINDS NIH HHS/ -- AI030165/AI/NIAID NIH HHS/ -- R01NS059991/NS/NINDS NIH HHS/ -- R01NS072248/NS/NINDS NIH HHS/ -- RC2-NS070-342/NS/NINDS NIH HHS/ -- U54NS065712/NS/NINDS NIH HHS/ -- Biotechnology and Biological Sciences Research Council/United Kingdom -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2012 Jul 27;337(6093):481-4. doi: 10.1126/science.1223899. Epub 2012 Jun 7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, University of Massachusetts Medical School, Worcester, MA 01605, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22678360" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Genetically Modified ; Apoptosis ; Armadillo Domain Proteins/analysis/*genetics/*physiology ; Axons/*physiology/ultrastructure ; Axotomy ; Cell Survival ; Cells, Cultured ; Cytoskeletal Proteins/analysis/*genetics/*physiology ; Denervation ; Drosophila/embryology/genetics/physiology ; Drosophila Proteins/analysis/*genetics/*physiology ; Mice ; Mutation ; Neurons/*physiology ; Sciatic Nerve/injuries/physiology ; Signal Transduction ; Superior Cervical Ganglion/cytology ; Tissue Culture Techniques ; *Wallerian Degeneration
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Long-term potentiation of neuron-glia synapses mediated by Ca2+-permeable AMPA receptors (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-06-10
    Description: Interactions between neurons and glial cells in the brain may serve important functions in the development, maintenance, and plasticity of neural circuits. Fast neuron-glia synaptic transmission has been found between hippocampal neurons and NG2 cells, a distinct population of macroglia-like cells widely distributed in the brain. We report that these neuron-glia synapses undergo activity-dependent modifications analogous to long-term potentiation (LTP) at excitatory synapses, a hallmark of neuronal plasticity. However, unlike the induction of LTP at many neuron-neuron synapses, both induction and expression of LTP at neuron-NG2 synapses involve Ca2+-permeable AMPA receptors on NG2 cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ge, Woo-Ping -- Yang, Xiu-Juan -- Zhang, Zhijun -- Wang, Hui-Kun -- Shen, Wanhua -- Deng, Qiu-Dong -- Duan, Shumin -- New York, N.Y. -- Science. 2006 Jun 9;312(5779):1533-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Neuroscience and Key Laboratory of Neurobiology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China. shumin@ion.ac.cn〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16763153" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/*metabolism ; Excitatory Postsynaptic Potentials ; Hippocampus/cytology ; In Vitro Techniques ; *Long-Term Potentiation ; Neuroglia/*physiology ; Neurons/*physiology ; Rats ; Receptors, AMPA/*physiology ; Synapses/*physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
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    PAPER CURRENT
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