Department of Pharmacology and Toxicology, Michigan State University, East Lansing, MI, 48824, USA.
Neurobiol Dis. 2010 Jun;38(3):405-13. doi: 10.1016/j.nbd.2010.02.013. Epub 2010 Mar 6.
In the CNS, ATP is released upon injury and promotes neuroproliferation via purinergic receptors. In the olfactory epithelium, ATP promotes the synthesis and release of neurotrophic factor NPY in neonates and induces neuroproliferation in neonatal and adult mice. We tested the hypothesis that NPY is involved in ATP-induced neuroproliferation in adult mice olfactory epithelium. Intranasal instillation of ATP significantly increased protein levels and number of NPY(+) cells. Pre-intranasal instillation of purinergic receptor antagonist PPADS significantly reduced ATP-induced upregulation of NPY. Intranasal instillation of NPY-Y1 receptor antagonist BIBP3226 following ATP instillation significantly inhibited the ATP-induced increase in BrdU incorporation, suggesting that NPY is released after ATP instillation and activates Y1 receptors to promote neuroproliferation. These data indicate that ATP initiates neuroproliferation via NPY upregulation, NPY release, and Y1 receptor activation, and suggests that the olfactory epithelium is good model to study neuroregenerative mechanisms in the CNS.
在中枢神经系统(CNS)中,损伤时会释放 ATP,并通过嘌呤能受体促进神经增殖。在嗅上皮中,ATP 促进神经营养因子 NPY 的合成和释放,并诱导新生和成年小鼠的神经增殖。我们检验了一个假设,即 NPY 参与成年小鼠嗅上皮中 ATP 诱导的神经增殖。鼻内滴注 ATP 可显著增加 NPY(+)细胞的蛋白水平和数量。鼻内预先滴注嘌呤能受体拮抗剂 PPADS 可显著降低 ATP 诱导的 NPY 上调。在 ATP 滴注后鼻内滴注 NPY-Y1 受体拮抗剂 BIBP3226 可显著抑制 ATP 诱导的 BrdU 掺入增加,表明 NPY 在 ATP 滴注后释放,并激活 Y1 受体促进神经增殖。这些数据表明,ATP 通过 NPY 上调、NPY 释放和 Y1 受体激活启动神经增殖,并表明嗅上皮是研究 CNS 神经再生机制的良好模型。