Morphotype-specific calcium signaling in human microglia
Journal of Neuroinflammation, vol. 21, pp. 175
Abstract
Abstract Background Key functions of Ca 2+ signaling in rodent microglia include monitoring the brain state as well as the surrounding neuronal activity and sensing the danger or damage in their vicinity. Microglial Ca 2+ dyshomeostasis is a disease hallmark in many mouse models of neurological disorders but the Ca 2+ signal properties of human microglia remain unknown. Methods We developed a novel genetically-encoded ratiometric Ca 2+ indicator, targeting microglial cells in the freshly resected human tissue, organotypically cultured tissue slices and analyzed in situ ongoing Ca 2+ signaling of decades-old microglia dwelling in their native microenvironment. Results The data revealed marked compartmentalization of Ca 2+ signals, with signal properties differing across the compartments and resident morphotypes. The basal Ca 2+ levels were low in ramified and high in ameboid microglia. The fraction of cells with ongoing Ca 2+ signaling, the fraction and the amplitude of process Ca 2+ signals and the duration of somatic Ca 2+ signals decreased when moving from ramified via hypertrophic to ameboid microglia. In contrast, the size of active compartments, the fraction and amplitude of somatic Ca 2+ signals and the duration of process Ca 2+ signals increased along this pathway.
Authors 12
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Affiliation as printed
Department of Neurophysiology, Institute of Physiology, Eberhard Karls University of Tübingen, Keplerstr. 15, 72074, Tübingen, Germany
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Affiliation as printed
Department of Neurophysiology, Institute of Physiology, Eberhard Karls University of Tübingen, Keplerstr. 15, 72074, Tübingen, Germany
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Hertie Institute for Clinical Brain Research · University of Tübingen
Affiliation as printed
Department of Neurology and Epileptology, Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany
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Max Planck Institute for Biological Intelligence
Affiliation as printed
Tools for Bio-Imaging, Max-Planck-Institute for Biological Intelligence, Martinsried, Germany
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Hertie Institute for Clinical Brain Research · University of Tübingen
Affiliation as printed
Department of Neurology and Epileptology, Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany
Department of Neurosurgery, University of Tübingen, Tübingen, Germany
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Affiliation as printed
Department of Neurophysiology, Institute of Physiology, Eberhard Karls University of Tübingen, Keplerstr. 15, 72074, Tübingen, Germany
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Universitätsklinikum Aachen · RWTH Aachen University
Affiliation as printed
Department of Epileptology, Neurology, RWTH Aachen University Hospital, Aachen, Germany
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Affiliation as printed
Department of Neurosurgery, RWTH Aachen University, Aachen, Germany
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Affiliation as printed
Department of Neurophysiology, Institute of Physiology, Eberhard Karls University of Tübingen, Keplerstr. 15, 72074, Tübingen, Germany
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University of Tübingen · The University of Texas Health Science Center at Houston
Affiliation as printed
Department of Anesthesiology, Critical Care and Pain Medicine, University of Texas Health Science Center at Houston, Houston, TX, USA
Department of Neurophysiology, Institute of Physiology, Eberhard Karls University of Tübingen, Keplerstr. 15, 72074, Tübingen, Germany
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Max Planck Institute for Biological Intelligence
Affiliation as printed
Tools for Bio-Imaging, Max-Planck-Institute for Biological Intelligence, Martinsried, Germany
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Olga Garaschuk corresponding
Affiliation as printed
Department of Neurophysiology, Institute of Physiology, Eberhard Karls University of Tübingen, Keplerstr. 15, 72074, Tübingen, Germany. olga.garaschuk@uni-tuebingen.de
Department of Neurophysiology, Institute of Physiology, Eberhard Karls University of Tübingen, Keplerstr. 15, 72074, Tübingen, Germany
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