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  • 1
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    Resting microglial cells are highly dynamic surveillants of brain parenchyma in vivo (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-04-16
    Description: Microglial cells represent the immune system of the mammalian brain and therefore are critically involved in various injuries and diseases. Little is known about their role in the healthy brain and their immediate reaction to brain damage. By using in vivo two-photon imaging in neocortex, we found that microglial cells are highly active in their presumed resting state, continually surveying their microenvironment with extremely motile processes and protrusions. Furthermore, blood-brain barrier disruption provoked immediate and focal activation of microglia, switching their behavior from patroling to shielding of the injured site. Microglia thus are busy and vigilant housekeepers in the adult brain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nimmerjahn, Axel -- Kirchhoff, Frank -- Helmchen, Fritjof -- New York, N.Y. -- Science. 2005 May 27;308(5726):1314-8. Epub 2005 Apr 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Abteilung Zellphysiologie, Max Planck Institut fur Medizinische Forschung, Jahnstrasse 29, 69120 Heidelberg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15831717" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Astrocytes/physiology/ultrastructure ; Bicuculline/pharmacology ; Blood-Brain Barrier ; Brain Injuries/physiopathology ; Capillaries/injuries ; Cell Movement ; Cell Surface Extensions/*physiology/ultrastructure ; GABA Antagonists/pharmacology ; Green Fluorescent Proteins ; Lasers ; Lipopolysaccharides/pharmacology ; Mice ; Mice, Transgenic ; Microglia/cytology/*physiology/*ultrastructure ; Microscopy, Fluorescence ; Neocortex/*cytology/*physiology ; Pseudopodia/physiology ; Sodium Channel Blockers/pharmacology ; Tetrodotoxin/pharmacology
    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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    TAM receptors regulate multiple features of microglial physiology (2016)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2016-04-07
    Description: Microglia are damage sensors for the central nervous system (CNS), and the phagocytes responsible for routine non-inflammatory clearance of dead brain cells. Here we show that the TAM receptor tyrosine kinases Mer and Axl regulate these microglial functions. We find that adult mice deficient in microglial Mer and Axl exhibit a marked accumulation of apoptotic cells specifically in neurogenic regions of the CNS, and that microglial phagocytosis of the apoptotic cells generated during adult neurogenesis is normally driven by both TAM receptor ligands Gas6 and protein S. Using live two-photon imaging, we demonstrate that the microglial response to brain damage is also TAM-regulated, as TAM-deficient microglia display reduced process motility and delayed convergence to sites of injury. Finally, we show that microglial expression of Axl is prominently upregulated in the inflammatory environment that develops in a mouse model of Parkinson's disease. Together, these results establish TAM receptors as both controllers of microglial physiology and potential targets for therapeutic intervention in CNS disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fourgeaud, Lawrence -- Traves, Paqui G -- Tufail, Yusuf -- Leal-Bailey, Humberto -- Lew, Erin D -- Burrola, Patrick G -- Callaway, Perri -- Zagorska, Anna -- Rothlin, Carla V -- Nimmerjahn, Axel -- Lemke, Greg -- DP2 NS083038/DP/NCCDPHP CDC HHS/ -- DP2 NS083038/NS/NINDS NIH HHS/ -- P30CA014195/CA/NCI NIH HHS/ -- R01 AI089824/AI/NIAID NIH HHS/ -- R01 AI101400/AI/NIAID NIH HHS/ -- R01 NS085296/NS/NINDS NIH HHS/ -- R01 NS085938/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2016 Apr 14;532(7598):240-4. doi: 10.1038/nature17630. Epub 2016 Apr 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Neurobiology Laboratory, The Salk Institute for Biological Studies, La Jolla, California 92037, USA. ; Instituto de Investigaciones Biomedicas Alberto Sols (CSIC-UAM), Madrid 28029, Spain. ; Waitt Advanced Biophotonics Center, The Salk Institute for Biological Studies, La Jolla, California 92037, USA. ; Joint Master in Neuroscience Program, University of Strasbourg, Strasbourg 67081, France. ; Department of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06520, USA. ; Immunobiology and Microbial Pathogenesis Laboratory, The Salk Institute for Biological Studies, La Jolla, California 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27049947" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Brain/blood supply/cytology/*metabolism/pathology ; Brain Injuries/metabolism/pathology ; Disease Models, Animal ; Female ; Inflammation/metabolism ; Intercellular Signaling Peptides and Proteins/metabolism ; Ligands ; Male ; Mice ; Microglia/*physiology ; Neurogenesis ; Parkinson Disease/metabolism ; Phagocytosis ; Protein S/metabolism ; Proto-Oncogene Proteins/deficiency/*metabolism ; Receptor Protein-Tyrosine Kinases/deficiency/*metabolism ; Signal Transduction ; Stem Cell Niche ; Up-Regulation
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 3
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    Fc{gamma} receptor IV and osteoclasts [Immunology] (2013)
    National Academy of Sciences
    Details
    Publication Date: 2013-06-26
    Description: Destruction of bone tissue by osteoclasts represents a severe pathological phenotype during inflammatory arthritis and results in joint pain and bone malformations. Previous studies have established the essential role of cytokines including TNFα and receptor–ligand interactions, such as the receptor activator of nuclear factor-kappa B–receptor activator of nuclear factor-kappa B...
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 4
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    Lentivirus-based genetic manipulations of cortical neurons and their optical and electrophysiological monitoring in vivo (2004)
    National Academy of Sciences
    Details
    Publication Date: 2004-12-17
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 5
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    Ultrafast neuronal imaging of dopamine dynamics with designed genetically encoded sensors (2018)
    American Association for the Advancement of Science (AAAS)
    In: Science
    Details
    Publication Date: 2018-06-29
    Description: Neuromodulatory systems exert profound influences on brain function. Understanding how these systems modify the operating mode of target circuits requires spatiotemporally precise measurement of neuromodulator release. We developed dLight1, an intensity-based genetically encoded dopamine indicator, to enable optical recording of dopamine dynamics with high spatiotemporal resolution in behaving mice. We demonstrated the utility of dLight1 by imaging dopamine dynamics simultaneously with pharmacological manipulation, electrophysiological or optogenetic stimulation, and calcium imaging of local neuronal activity. dLight1 enabled chronic tracking of learning-induced changes in millisecond dopamine transients in mouse striatum. Further, we used dLight1 to image spatially distinct, functionally heterogeneous dopamine transients relevant to learning and motor control in mouse cortex. We also validated our sensor design platform for developing norepinephrine, serotonin, melatonin, and opioid neuropeptide indicators.
    Keywords: Neuroscience, Online Only
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Geosciences , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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