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Updated: Jun 24, 2026

Two-photon Imaging of Microglial Processes' Attraction Toward ATP or Serotonin in Acute Brain Slices
Published on: January 31, 2019
Glutamate induces directed chemotaxis of microglia
Guo Jun Liu1, Rajini Nagarajah, Richard B Banati
1The Neurobiology Laboratory, Brain and Mind Research Institute, University of Sydney, NSW, Australia.
Abstract:
Microglia in the brain possess dynamic processes that continually sample the surrounding parenchyma and respond to local insults by rapidly converging on the site of an injury. One of the chemotaxic agents responsible for this response is ATP. Here we show that the transmitter glutamate is another such chemotaxic agent. Microglia exposed to glutamate increase their cell membrane ruffling and migrate to a source of glutamate in cell culture and in spinal cord slices. This chemotaxis is meditated by alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) and metabotropic glutamate receptors on the microglia. Chemotaxis is dependent on redistribution of actin filaments in the cells and on tubulin following receptor activation. Thus glutamate, which is released at synapses as well as from damaged cells, can mediate rapid chemotaxic responses from microglial cells.
Insights
Glutamate, a brain transmitter, acts as a chemotaxic agent, guiding microglia to injury sites. This microglial response involves specific glutamate receptors and cytoskeletal changes, aiding in brain injury repair.
Area of Science:
- Neuroscience
- Immunology
- Cell Biology
Background:
- Microglia are brain immune cells that respond to injury.
- ATP is a known chemotaxic agent for microglia.
- The role of other neurotransmitters in microglial chemotaxis is less understood.
Purpose of the Study:
- To investigate if glutamate acts as a chemotaxic agent for microglia.
- To identify the receptors and cellular mechanisms involved in glutamate-induced microglial migration.
Main Methods:
- Microglial cell cultures and spinal cord slices were used.
- Cells were exposed to glutamate, and migration was observed.
- Specific glutamate receptor antagonists (AMPA and mGluR) were employed.
- Changes in actin and tubulin cytoskeleton were analyzed.
Main Results:
- Glutamate exposure induced microglial membrane ruffling and migration towards the glutamate source.
- This chemotaxis was mediated by alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) and metabotropic glutamate receptors.
- Glutamate-induced migration depended on the redistribution of actin filaments and tubulin.
Conclusions:
- Glutamate is identified as a novel chemotaxic agent for microglia.
- Glutamate signaling via AMPA and mGluRs plays a role in microglial injury response.
- This finding highlights glutamate's role in mediating rapid microglial responses at synapses and sites of cell damage.
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