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Here we show that MRF\u20101 is released from cultured rat microglia, and its release is greatly enhanced under inflammatory conditions. When microglia were treated with ATP, the amount of MRF\u20101 that was released increased 10\u2010fold compared to the basal level of release. Enhanced MRF\u20101 release was induced within 10 min and peaked within 1 h; after \u223c 4 h, the MRF\u20101 release had returned to normal. MRF\u20101 release was stimulated by 2\u2010methyl\u2010thio\u2010ATP (five\u2010fold) and a P2X<jats:sub>7<\/jats:sub> selective agonist, 2\u2032\u2010 and 3\u2032\u2010<jats:italic>O<\/jats:italic>\u2010(4\u2010benzoylbenzoyl)\u2010ATP (ten\u2010fold). Moreover, the ATP\u2010stimulated MRF\u20101 release was inhibited by a P2X<jats:sub>7<\/jats:sub> selective antagonist, oxidized ATP (oATP), and also under a Ca<jats:sup>2+<\/jats:sup>\u2010free condition. These results indicate that the effects of ATP are dependent on Ca<jats:sup>2+<\/jats:sup> influx through P2X<jats:sub>7<\/jats:sub> receptors. MRF\u20101 release was enhanced by Ca<jats:sup>2+<\/jats:sup>\u2010ionophore A23187 (sixfold), thapsigargin (threefold); however, it was not enhanced by glutamate or lipopolysaccharide. Moreover, a platelet\u2010activating factor enhanced microglial MRF\u20101 release in a dose\u2010dependent manner. We also showed that a conditioned medium from cerebellar granule neurons undergoing apoptosis markedly increased MRF\u20101 release from microglia; that effect was significantly inhibited by oATP. These results indicate that selective inflammatory stimulations, including ATP and PAF, enhance MRF\u20101 release from microglia through a Ca<jats:sup>2+<\/jats:sup>\u2010dependent mechanism and suggest that MRF\u20101 may play a role in cell\u2010cell interactions under inflammatory conditions. 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