Glutamate Induces Directed Chemotaxis of Microglia

Eur J Neurosci. 2009 Mar;29(6):1108-18. doi: 10.1111/j.1460-9568.2009.06659.x.

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.

MeSH terms

  • Analysis of Variance
  • Animals
  • Animals, Newborn
  • CD11b Antigen / metabolism
  • Cell Culture Techniques / methods
  • Cell Membrane / drug effects
  • Cells, Cultured
  • Chemotaxis / drug effects*
  • Cytochalasin D / pharmacology
  • Drug Interactions
  • Excitatory Amino Acid Agents / pharmacology
  • Glutamic Acid / pharmacology*
  • Microglia / cytology
  • Microglia / drug effects*
  • Microglia / physiology*
  • Nocodazole / pharmacology
  • Nucleic Acid Synthesis Inhibitors / pharmacology
  • Rats
  • Rats, Sprague-Dawley
  • Spinal Cord / cytology
  • Time Factors
  • Tubulin Modulators / pharmacology
  • cdc42 GTP-Binding Protein / metabolism

Substances

  • CD11b Antigen
  • Excitatory Amino Acid Agents
  • Nucleic Acid Synthesis Inhibitors
  • Tubulin Modulators
  • Cytochalasin D
  • Glutamic Acid
  • cdc42 GTP-Binding Protein
  • Nocodazole