Spontaneous Ca2+ transients in mouse microglia

Laura Korvers1, Amanda de Andrade Costa1, Martin Mersch1

  • 1Max-Delbrueck-Centrum for Molecular Medicine (MDC) in the Helmholtz Association, Cellular Neurosciences, Robert-Roessle-Str. 10, 13092 Berlin, Germany.

Cell Calcium
|October 5, 2016
PubMed

Insights

Resident immune cells in the brain, microglia, exhibit spontaneous calcium (Ca2+) signaling. This signaling originates from internal stores and is crucial for microglial homeostasis and function.

Area of Science:

  • Neuroimmunology
  • Cellular Physiology
  • Calcium Signaling

Background:

  • Microglia are key immune cells in the central nervous system.
  • Their functions are intricately linked to intracellular calcium (Ca2+) signaling pathways.

Purpose of the Study:

  • To investigate spontaneous intracellular Ca2+ transients in isolated mouse microglia.
  • To determine the source and triggers of these Ca2+ events.

Main Methods:

  • Isolation and purification of mouse microglia (fresh and cultured).
  • Measurement of intracellular Ca2+ using fluorescence imaging.
  • Pharmacological inhibition of phospholipase C (PLC) and inositol-1,4,5-trisphosphate receptors (IP3Rs).
  • Assessment of Ca2+ signaling in LPS-stimulated and glioma-associated microglia.

Main Results:

  • Isolated microglia display spontaneous, transient Ca2+ elevations (10-20 seconds duration, 5-10 events/hour/cell).
  • These events depend on internal Ca2+ stores (endoplasmic reticulum) and are independent of extracellular Ca2+.
  • Autocrine ATP release and P2Y receptor activation do not trigger these transients.
  • Spontaneous Ca2+ transients are altered in LPS-stimulated and glioma-associated microglia.

Conclusions:

  • Spontaneous Ca2+ transients in microglia originate from intracellular stores.
  • These signaling events are a fundamental aspect of microglial cellular homeostasis.
  • Understanding these transients is vital for comprehending both normal and pathological microglial functions.

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