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  • 1
    Publication Date: 2008-05-20
    Description: Development of axonal tracts requires interactions between growth cones and the environment. Tracts such as the anterior commissure and internal capsule are defective in mice with null mutation of Celsr3. We generated a conditional Celsr3 allele, allowing regional inactivation. Inactivation in telencephalon, ventral forebrain, or cortex demonstrated essential roles for Celsr3 in neurons that project axons to the anterior commissure and subcerebral targets, as well as in cells that guide axons through the internal capsule. When Celsr3 was inactivated in cortex, subcerebral projections failed to grow, yet corticothalamic axons developed normally, indicating that besides guidepost cells, additional Celsr3-independent cues can assist their progression. These observations provide in vivo evidence that Celsr3-mediated interactions between axons and guidepost cells govern axonal tract formation in mammals.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2746700/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2746700/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhou, Libing -- Bar, Isabelle -- Achouri, Younes -- Campbell, Kenneth -- De Backer, Olivier -- Hebert, Jean M -- Jones, Kevin -- Kessaris, Nicoletta -- de Rouvroit, Catherine Lambert -- O'Leary, Dennis -- Richardson, William D -- Goffinet, Andre M -- Tissir, Fadel -- G0501173/Medical Research Council/United Kingdom -- G0800575/Medical Research Council/United Kingdom -- G9708005/Medical Research Council/United Kingdom -- R01 MH086147/MH/NIMH NIH HHS/ -- R01 MH086147-05/MH/NIMH NIH HHS/ -- R37 NS031558/NS/NINDS NIH HHS/ -- R37 NS031558-15/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2008 May 16;320(5878):946-9. doi: 10.1126/science.1155244.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Developmental Neurobiology, Universite Catholique de Louvain, 1200 Bruxelles, Belgique.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18487195" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/*physiology ; Cadherins/*genetics/*physiology ; Cerebral Cortex/cytology/embryology ; Female ; Gene Silencing ; Internal Capsule/cytology/embryology/physiology ; Male ; Mice ; Neural Pathways/*embryology/physiology ; Neurons/*physiology ; Prosencephalon/cytology/*embryology/physiology ; Receptors, Cell Surface/*genetics/*physiology ; Septal Nuclei/embryology/physiology ; Thalamus/cytology/embryology ; Tissue Culture Techniques
    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
    Publication Date: 2012-06-30
    Description: Astrocytes, the most abundant cell population in the central nervous system (CNS), are essential for normal neurological function. We show that astrocytes are allocated to spatial domains in mouse spinal cord and brain in accordance with their embryonic sites of origin in the ventricular zone. These domains remain stable throughout life without evidence of secondary tangential migration, even after acute CNS injury. Domain-specific depletion of astrocytes in ventral spinal cord resulted in abnormal motor neuron synaptogenesis, which was not rescued by immigration of astrocytes from adjoining regions. Our findings demonstrate that region-restricted astrocyte allocation is a general CNS phenomenon and reveal intrinsic limitations of the astroglial response to injury.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4059181/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4059181/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tsai, Hui-Hsin -- Li, Huiliang -- Fuentealba, Luis C -- Molofsky, Anna V -- Taveira-Marques, Raquel -- Zhuang, Helin -- Tenney, April -- Murnen, Alice T -- Fancy, Stephen P J -- Merkle, Florian -- Kessaris, Nicoletta -- Alvarez-Buylla, Arturo -- Richardson, William D -- Rowitch, David H -- G0501173/Medical Research Council/United Kingdom -- G0800575/Medical Research Council/United Kingdom -- R01 NS028478/NS/NINDS NIH HHS/ -- R37 HD032116/HD/NICHD NIH HHS/ -- Howard Hughes Medical Institute/ -- Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2012 Jul 20;337(6092):358-62. doi: 10.1126/science.1222381. Epub 2012 Jun 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, University of California San Francisco, San Francisco, CA 94143, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22745251" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Astrocytes/*physiology ; Bacterial Proteins/metabolism ; Basic Helix-Loop-Helix Transcription Factors/genetics ; Brain/abnormalities/*cytology/physiology ; Brain Injuries/physiopathology ; *Cell Movement ; Green Fluorescent Proteins ; Homeodomain Proteins/metabolism ; Integrases/genetics ; Luminescent Proteins/metabolism ; Mice ; Mice, Transgenic ; Motor Neurons/*physiology ; Nerve Tissue Proteins/genetics ; Proteins/metabolism ; RNA, Untranslated ; Spinal Cord/abnormalities/*cytology/physiology ; Spinal Cord Injuries/physiopathology ; Synapses/*physiology ; Transcription Factors/metabolism ; Transcription, Genetic
    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
    Publication Date: 2014-10-18
    Description: Myelin-forming oligodendrocytes (OLs) are formed continuously in the healthy adult brain. In this work, we study the function of these late-forming cells and the myelin they produce. Learning a new motor skill (such as juggling) alters the structure of the brain's white matter, which contains many OLs, suggesting that late-born OLs might contribute to motor learning. Consistent with this idea, we show that production of newly formed OLs is briefly accelerated in mice that learn a new skill (running on a "complex wheel" with irregularly spaced rungs). By genetically manipulating the transcription factor myelin regulatory factor in OL precursors, we blocked production of new OLs during adulthood without affecting preexisting OLs or myelin. This prevented the mice from mastering the complex wheel. Thus, generation of new OLs and myelin is important for learning motor skills.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McKenzie, Ian A -- Ohayon, David -- Li, Huiliang -- de Faria, Joana Paes -- Emery, Ben -- Tohyama, Koujiro -- Richardson, William D -- 100269/Wellcome Trust/United Kingdom -- G0800575/Medical Research Council/United Kingdom -- Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2014 Oct 17;346(6207):318-22. doi: 10.1126/science.1254960.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Wolfson Institute for Biomedical Research, University College London, Gower Street, London WC1E 6BT, UK. ; Department of Anatomy and Neuroscience and the Florey Institute for Neuroscience and Mental Health, University of Melbourne, Melbourne, Victoria 3010, Australia. ; The Center for Electron Microscopy and Bio-Imaging Research, Iwate Medical University, 19-1 Uchimuru, Morioka, Iwate 020-8505, Japan. ; The Wolfson Institute for Biomedical Research, University College London, Gower Street, London WC1E 6BT, UK. w.richardson@ucl.ac.uk.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25324381" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*cytology/metabolism ; *Cell Proliferation ; Gene Deletion ; Humans ; *Learning ; Male ; Mental Recall ; Mice ; Mice, Transgenic ; Motor Skills/*physiology ; Myelin Sheath/genetics/*metabolism ; Oligodendroglia/cytology/metabolism/*physiology ; Synaptic Transmission ; Transcription Factors/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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  • 4
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Journal of the American Chemical Society 30 (1908), S. 911-912 
    ISSN: 1520-5126
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Journal of the American Chemical Society 29 (1907), S. 1757-1767 
    ISSN: 1520-5126
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Journal of the American Chemical Society 30 (1908), S. 421-422 
    ISSN: 1520-5126
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Journal of the American Chemical Society 30 (1908), S. 1044-1045 
    ISSN: 1520-5126
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Journal of the American Chemical Society 30 (1908), S. 1191-1192 
    ISSN: 1520-5126
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 9
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Journal of the American Chemical Society 30 (1908), S. 1515-1564 
    ISSN: 1520-5126
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Journal of the American Chemical Society 29 (1907), S. 1314-1315 
    ISSN: 1520-5126
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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