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Parenchymal microglia are the principal immune cells of the brain. Time-lapse two-photon imaging of GFP-labeled microglia demonstrates that the fine termini of microglial processes are highly dynamic in the intact mouse cortex. Upon traumatic brain injury, microglial processes rapidly and autonomously converge on the site of injury without cell body movement, establishing a potential barrier between the healthy and injured tissue. This rapid chemotactic response can be mimicked by local injection of ATP and can be inhibited by the ATP-hydrolyzing enzyme apyrase or by blockers of G protein-coupled purinergic receptors and connexin channels, which are highly expressed in astrocytes. The baseline motility of microglial processes is also reduced significantly in the presence of apyrase and connexin channel inhibitors. Thus, extracellular ATP regulates microglial branch dynamics in the intact brain, and its release from the damaged tissue and surrounding astrocytes mediates a rapid microglial response towards injury.

Original publication




Journal article


Nature neuroscience

Publication Date





752 - 758


Molecular Neurobiology Program, Department of Physiology and Neuroscience, New York University School of Medicine, 540 First Avenue, New York, New York 10016, USA.


Brain, Astrocytes, Microglia, Animals, Mice, Transgenic, Mice, Brain Injuries, Gliosis, Apyrase, Green Fluorescent Proteins, Connexins, Receptors, Purinergic P2, Adenosine Triphosphate, Reaction Time, Cell Communication, Signal Transduction, Chemotaxis, Phagocytosis, Receptors, Purinergic P2Y1, Purinergic P2 Receptor Antagonists