Long-Range Ca(2+) Waves Transmit Brain-Damage Signals to Microglia
- Authors
- Sieger, D., Moritz, C., Ziegenhals, T., Prykhozhij, S., and Peri, F.
- ID
- ZDB-PUB-120529-46
- Date
- 2012
- Source
- Developmental Cell 22(6): 1138-1148 (Journal)
- Registered Authors
- Peri, Francesca, Prykhozhij, Sergey, Sieger, Dirk
- Keywords
- none
- MeSH Terms
-
- Calcium Signaling/drug effects
- Calcium Signaling/physiology*
- Laser Therapy
- Adenosine Triphosphate/physiology
- Animals
- Zebrafish/growth & development
- Zebrafish/physiology
- Glutamic Acid/physiology
- Cell Death/drug effects
- Cell Death/physiology
- Microglia/drug effects
- Microglia/physiology*
- Chelating Agents/metabolism
- Cell Movement/drug effects
- Cell Movement/physiology
- Brain Injuries/physiopathology*
- PubMed
- 22632801 Full text @ Dev. Cell
Microglia are the resident phagocytes of the brain that are responsible for the clearance of injured neurons, an essential step in subsequent tissue regeneration. How death signals are controlled both in space and time to attract these cells toward the site of injury is a topic of great interest. To this aim, we have used the optically transparent zebrafish larval brain and identified rapidly propagating Ca2+ waves that determine the range of microglial responses to neuronal cell death. We show that while Ca2+-mediated microglial responses require ATP, the spreading of intercellular Ca2+ waves is ATP independent. Finally, we identify glutamate as a potent inducer of Ca2+-transmitted microglial attraction. Thus, this real-time analysis reveals the existence of a mechanism controlling microglial targeted migration to neuronal injuries that is initiated by glutamate and proceeds across the brain in the form of a Ca2+ wave.