The P2Y12 receptor regulates microglial activation by extracellular nucleotides by Sharon E. Haynes, 2006. This study investigates the role of the P2Y12 receptor in microglial activation in response to extracellular nucleotides. Microglia, the primary immune cells of the central nervous system (CNS), become activated following injury, leading to migration and process extension towards sites of damage. The study shows that microglia lacking P2Y12 receptors exhibit normal baseline motility but are unable to polarize, migrate, or extend processes towards nucleotides in vitro or in vivo. P2Y12 expression is robust in the resting state but decreases after microglial activation, suggesting that P2Y12 is a primary site for nucleotide-induced chemotaxis during early stages of CNS injury. The study also highlights the importance of P2Y12 in microglial morphological responses to tissue injury. The research was conducted in collaboration with researchers from COR Therapeutics, and mice genetically engineered to lack P2Y12 receptors were used. The study confirms that P2Y12 is an essential component of the signaling pathway through which extracellular purines promote directed microglial movement following CNS injury. The findings suggest that P2Y12 signaling is most relevant during early stages of microglial activation. The study also explores the pharmacology of P2Y12 and P2Y13 receptors, showing that they share similar pharmacological profiles but differ in their sensitivity to certain ligands. The research provides insights into the role of P2Y12 in microglial biology and its potential as a molecular marker for visualizing brain microglia in the ramified state. The study was published in Nature Neuroscience and is licensed for use under specific terms.The P2Y12 receptor regulates microglial activation by extracellular nucleotides by Sharon E. Haynes, 2006. This study investigates the role of the P2Y12 receptor in microglial activation in response to extracellular nucleotides. Microglia, the primary immune cells of the central nervous system (CNS), become activated following injury, leading to migration and process extension towards sites of damage. The study shows that microglia lacking P2Y12 receptors exhibit normal baseline motility but are unable to polarize, migrate, or extend processes towards nucleotides in vitro or in vivo. P2Y12 expression is robust in the resting state but decreases after microglial activation, suggesting that P2Y12 is a primary site for nucleotide-induced chemotaxis during early stages of CNS injury. The study also highlights the importance of P2Y12 in microglial morphological responses to tissue injury. The research was conducted in collaboration with researchers from COR Therapeutics, and mice genetically engineered to lack P2Y12 receptors were used. The study confirms that P2Y12 is an essential component of the signaling pathway through which extracellular purines promote directed microglial movement following CNS injury. The findings suggest that P2Y12 signaling is most relevant during early stages of microglial activation. The study also explores the pharmacology of P2Y12 and P2Y13 receptors, showing that they share similar pharmacological profiles but differ in their sensitivity to certain ligands. The research provides insights into the role of P2Y12 in microglial biology and its potential as a molecular marker for visualizing brain microglia in the ramified state. The study was published in Nature Neuroscience and is licensed for use under specific terms.