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Related Concept Videos

Calmodulin-dependent Signaling01:16

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Calmodulin (CaM) is a calcium-binding protein in eukaryotes that controls various calcium-regulated cellular processes. It has four calcium-binding sites that bind calcium to form the calcium-calmodulin ( Ca2+-CaM) complex. GPCR stimulation increases the calcium levels in the cells that bind to CaM and induces a conformational change.
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Calcium is an essential signaling molecule required for various cellular functions. Calcium pumps and ion channels on cell and organellar membranes, such as those on the endoplasmic reticulum (ER), regulate calcium concentrations inside the cell. They remain closed, keeping the cytosolic calcium levels low at a resting state.
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Isolation of Cortical Microglia with Preserved Immunophenotype and Functionality From Murine Neonates
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Calcium Signalling in Microglia.

Olga Garaschuk1, Alexei Verkhratsky2,3,4,5

  • 1Institute of Physiology, Department Neurophysiology, Eberhard Karls University of Tübingen, Tübingen, Germany. olga.garaschuk@uni-tuebingen.de.

Advances in Neurobiology
|August 29, 2024
PubMed
Summary
This summary is machine-generated.

Microglial cells use intracellular calcium (Ca2+) signals to sense brain changes. These signals, involving specific channels and pathways, adapt to maintain brain health and neuroprotection.

Keywords:
Calcium signallingMetabotropic receptorsMicrogliaPurinoceptorsTRP channels

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Area of Science:

  • Neuroscience
  • Cell Biology

Background:

  • Microglia are key immune cells in the brain.
  • Intracellular calcium (Ca2+) signaling is fundamental to microglial cell function and excitability.
  • Ca2+ signals are dynamic, responding to physiological and pathological stimuli.

Purpose of the Study:

  • To elucidate the role of intracellular Ca2+ signaling in microglial responses.
  • To highlight the Ca2+ signaling pathways crucial for microglial adaptive capabilities.
  • To connect microglial Ca2+ dynamics to neuroprotection in diseases.

Main Methods:

  • Analysis of Ca2+ signaling pathways in microglial cells.
  • Investigation of Ca2+ stores in the endoplasmic reticulum.
  • Examination of plasmalemmal Ca2+ entry via channels like TRP, ORAI, and P2X receptors.
  • Exploration of the link between TREM2 signaling and microglial Ca2+ dynamics.

Main Results:

  • Intracellular Ca2+ signals are the basis of microglial excitability.
  • Ca2+ signal parameters are determined by signaling toolkits that adapt with age and context.
  • Key pathways involve endoplasmic reticulum Ca2+ stores and plasmalemmal Ca2+ entry through various channels.
  • Microglial Ca2+ dynamics are integrated with TREM2 signaling, promoting neuroprotection.

Conclusions:

  • Microglial Ca2+ signals are essential for sensing brain dyshomeostasis and pathological insults.
  • Adaptive changes in Ca2+ signaling toolkits enhance microglial protective functions.
  • Understanding microglial Ca2+ dynamics is critical for neurodegenerative disease research.