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In this study, we investigated whether the microglial K<jats:sub>ATP<\/jats:sub>\u2010channel directly influences the activation of neural precursor cells (NPCs) from the subventricular zone using transgenic <jats:italic>Csf1r\u2010GFP<\/jats:italic> mice. <jats:italic>In vitro<\/jats:italic> exposure of NPCs to lipopolysaccharide and interferon\u2010gamma resulted in a significant decrease in precursor cell number. The complete removal of microglia from the culture or exposure to enriched microglia culture also decreased the precursor cell number. The addition of glibenclamide rescued the negative effects of enriched microglia on neurosphere formation and promoted a \u223c20% improvement in precursor cell number. Similar results were found using microglial\u2010conditioned media from isolated microglia. Using primary mixed glial and pure microglial cultures, glibenclamide specifically targeted reactive microglia to restore neurogenesis and increased the microglial production of the chemokine monocyte chemoattractant protein\u20101 (MCP\u20101). These findings provide the first direct evidence that the microglial K<jats:sub>ATP<\/jats:sub>\u2010channel is a regulator of the proliferation of NPCs under inflammatory conditions. 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