Abstract：
:Microglia are primary immune sentinels of the CNS. Following injury, these cells migrate or extend processes toward sites of tissue damage. CNS injury is accompanied by release of nucleotides, serving as signals for microglial activation or chemotaxis. Microglia express several purinoceptors, including a G(i)-coupled subtype that has been implicated in ATP- and ADP-mediated migration in vitro. Here we show that microglia from mice lacking G(i)-coupled P2Y(12) receptors exhibit normal baseline motility but are unable to polarize, migrate or extend processes toward nucleotides in vitro or in vivo. Microglia in P2ry(12)(-/-) mice show significantly diminished directional branch extension toward sites of cortical damage in the living mouse. Moreover, P2Y(12) expression is robust in the 'resting' state, but dramatically reduced after microglial activation. These results imply that P2Y(12) is a primary site at which nucleotides act to induce microglial chemotaxis at early stages of the response to local CNS injury.
journal_name
Nat Neuroscijournal_title
Nature neuroscienceauthors
Haynes SE,Hollopeter G,Yang G,Kurpius D,Dailey ME,Gan WB,Julius Ddoi
10.1038/nn1805subject
Has Abstractpub_date
2006-12-01 00:00:00pages
1512-9issue
12eissn
1097-6256issn
1546-1726pii
nn1805journal_volume
9pub_type
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