Neural and oligodendrocyte precursor cells (NPCs and OPCs) in the subventricular zone (SVZ) of the brain contribute to oligodendrogenesis throughout life, in part due to direct regulation by chemokines. The role of the chemokine fractalkine is well established in microglia; however, the effect of fractalkine on SVZ precursor cells is unknown. We show that murine SVZ NPCs and OPCs express the fractalkine receptor (CX3CR1) and bind fractalkine. Exogenous fractalkine directly enhances OPC and oligodendrocyte genesis from SVZ NPCs in vitro. Infusion of fractalkine into the lateral ventricle of adult NPC lineage-tracing mice leads to increased newborn OPC and oligodendrocyte formation in vivo. We also show that OPCs secrete fractalkine and that inhibition of endogenous fractalkine signaling reduces oligodendrocyte formation in vitro. Finally, we show that fractalkine signaling regulates oligodendrogenesis in cerebellar slices ex vivo. In summary, we demonstrate a novel role for fractalkine signaling in regulating oligodendrocyte genesis from postnatal CNS precursor cells.

脑室下区 (SVZ) 中的神经和少突胶质前体细胞 (NPCs 和 OPCs) 有助于终生少突胶质细胞的形成，部分原因是趋化因子的直接调节。趋化因子 fractalkine 的作用在小胶质细胞中得到了很好的证实。然而，fractalkine 对 SVZ 前体细胞的影响尚不清楚。我们显示鼠 SVZ NPC 和 OPCs 表达 fractalkine 受体 (CX3CR1) 并结合 fractalkine。外源性fractalkine在体外直接增强 SVZ NPCs 的 OPC 和少突胶质细胞的发生。将fractalkine注入成年NPC谱系追踪小鼠的侧脑室导致体内新生OPC和少突胶质细胞形成增加. 我们还表明，OPCs 分泌 fractalkine，抑制内源性 fractalkine 信号传导可减少体外少突胶质细胞的形成。最后，我们表明，fractalkine 信号传导调节离体小脑切片中的少突胶质细胞生成。总之，我们证明了 fractalkine 信号传导在调节出生后 CNS 前体细胞的少突胶质细胞发生中的新作用。