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Early Ischemia and Ionic ImbalanceWithin minutes of spinal cord injury, a secondary cascade begins, progressing over hours to weeks. Vascular damage reduces blood flow, causing ischemia and mitochondrial dysfunction. ATP depletion leads to ion pump failure, membrane depolarization, sodium influx, potassium efflux, and water accumulation, resulting in cellular swelling. Increased intracellular calcium further disrupts mitochondria and accelerates cellular injury.Excitotoxicity and Neuronal...
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If over time, all...
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Related Experiment Video

Updated: May 22, 2026

Measurement of Total Calcium in Neurons by Electron Probe X-ray Microanalysis
11:42

Measurement of Total Calcium in Neurons by Electron Probe X-ray Microanalysis

Published on: November 20, 2013

Long-range Ca2+ waves transmit brain-damage signals to microglia.

Dirk Sieger1, Christian Moritz, Thomas Ziegenhals

  • 1EMBL Heidelberg, Meyerhofstraße 1, 69117 Heidelberg, Germany.

Developmental Cell
|May 29, 2012
PubMed
Summary

Brain immune cells, microglia, migrate to injury sites via calcium (Ca2+) waves. Glutamate initiates these waves, guiding microglia to clear damaged neurons for tissue repair.

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Related Experiment Videos

Last Updated: May 22, 2026

Measurement of Total Calcium in Neurons by Electron Probe X-ray Microanalysis
11:42

Measurement of Total Calcium in Neurons by Electron Probe X-ray Microanalysis

Published on: November 20, 2013

Imaging Mitochondrial Ca2+ Uptake in Astrocytes and Neurons using Genetically Encoded Ca2+ Indicators (GECIs)
07:46

Imaging Mitochondrial Ca2+ Uptake in Astrocytes and Neurons using Genetically Encoded Ca2+ Indicators (GECIs)

Published on: January 22, 2022

Area of Science:

  • Neuroscience
  • Cell Biology
  • Developmental Biology

Background:

  • Microglia, the brain's immune cells, clear injured neurons for tissue regeneration.
  • Understanding how death signals spatially and temporally guide microglia to injury sites is crucial.

Purpose of the Study:

  • To investigate the real-time mechanisms controlling microglial migration to neuronal injury sites.
  • To identify signaling molecules and pathways involved in microglial response to cell death.

Main Methods:

  • Utilized the optically transparent zebrafish larval brain for real-time imaging.
  • Analyzed calcium (Ca2+) waves and their role in microglial responses.
  • Investigated the involvement of ATP and glutamate in the signaling cascade.

Main Results:

  • Identified rapidly propagating Ca2+ waves that dictate the extent of microglial response to neuronal death.
  • Demonstrated that Ca2+-mediated microglial responses depend on ATP, but Ca2+ wave propagation is ATP-independent.
  • Identified glutamate as a key inducer of Ca2+-transmitted microglial attraction.

Conclusions:

  • A novel mechanism for microglial-targeted migration to neuronal injuries has been revealed.
  • This process is initiated by glutamate and propagates as a Ca2+ wave across the brain.
  • This finding provides insights into brain repair and regeneration processes.