Distinct signatures of calcium activity in brain mural cells

eLife, Vol. 10 (2021)

Mots clés
Auteurs
  • Chaim Glück
  • Institute of Pharmacology and Toxicology, University of Zurich, Zürich, Switzerland; Neuroscience Center Zurich, University and ETH Zurich, Zurich, Switzerland
  • Kim David Ferrari
  • Institute of Pharmacology and Toxicology, University of Zurich, Zürich, Switzerland; Neuroscience Center Zurich, University and ETH Zurich, Zurich, Switzerland
  • Noemi Binini
  • Institute of Pharmacology and Toxicology, University of Zurich, Zürich, Switzerland; Neuroscience Center Zurich, University and ETH Zurich, Zurich, Switzerland
  • Annika Keller
  • Neuroscience Center Zurich, University and ETH Zurich, Zurich, Switzerland; Department of Neurosurgery, University of Zurich, Schlieren, Switzerland
  • Aiman S Saab
  • Institute of Pharmacology and Toxicology, University of Zurich, Zürich, Switzerland; Neuroscience Center Zurich, University and ETH Zurich, Zurich, Switzerland
  • Jillian L Stobart
  • Institute of Pharmacology and Toxicology, University of Zurich, Zürich, Switzerland; Rady Faculty of Health Sciences, College of Pharmacy, Winnipeg, Canada
  • Bruno Weber
  • Institute of Pharmacology and Toxicology, University of Zurich, Zürich, Switzerland; Neuroscience Center Zurich, University and ETH Zurich, Zurich, Switzerland

Résumé

Pericytes have been implicated in various neuropathologies, yet little is known about their function and signaling pathways in health. Here, we characterized calcium dynamics of cortical mural cells in anesthetized or awake Pdgfrb-CreERT2;Rosa26< LSL-GCaMP6s > mice and in acute brain slices. Smooth muscle cells (SMCs) and ensheathing pericytes (EPs), also named as terminal vascular SMCs, revealed similar calcium dynamics in vivo. In contrast, calcium signals in capillary pericytes (CPs) were irregular, higher in frequency, and occurred in cellular microdomains. In the absence of the vessel constricting agent U46619 in acute slices, SMCs and EPs revealed only sparse calcium signals, whereas CPs retained their spontaneous calcium activity. Interestingly, chemogenetic activation of neurons in vivo and acute elevations of extracellular potassium in brain slices strongly decreased calcium activity in CPs. We propose that neuronal activation and an extracellular increase in potassium suppress calcium activity in CPs, likely mediated by Kir2.2 and KATP channels.

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