Nitric oxide acts directly in the presynaptic neuron to produce long-term potentiation in cultured hippocampal neurons
Nitric oxide acts directly in the presynaptic neuron to produce long-term potentiation in cultured hippocampal neurons
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DOI：
10.1016/s0092-8674(00)81797-3
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发表时间：
1996-12-13
期刊：
影响因子：
64.5
通讯作者：
Hawkins, RD
中科院分区：
文献类型：
--
作者：
Arancio, O;Kiebler, M;Hawkins, RD
一氧化氮 (NO) 被认为在海马 CA1 区的长时程增强 (LTP) 过程中充当逆行信使，但突触前末梢的不可接近性阻碍了对这一假设的明确检验。因为在培养的海马神经元中突触的两侧都是可接近的，所以我们使用这种制剂来研究 NO 的作用。我们在细胞内或细胞外应用 NO 清除剂、NO 合酶抑制剂和非膜渗透性 NO 供体（仅在紫外光光解时释放 NO）后检查了 LTP。我们的结果表明，NO 在突触后神经元中产生，穿过细胞外间隙，直接在突触前神经元中起作用，产生长时程增强作用，支持了 NO 在 LTP 期间充当逆行信使的假设。
Nitric oxide (NO) has been proposed to act as a retrograde messenger during long-term potentiation (LTP) in the CA1 region of hippocampus, but the inaccessibility of the presynaptic terminal has prevented a definitive test of this hypothesis. Because both sides of the synapse are accessible in cultured hippocampal neurons, we have used this preparation to investigate the role of NO. We examined LTP following intra- or extracellular application of an NO scavanger, an inhibitor of NO synthase, and a membrane-impermeant NO donor that releases NO only upon photolysis with UV light. Our results indicate that NO is produced in the postsynaptic neuron, travels through the extracellular space, and acts directly in the presynaptic neuron to produce long-term potentiation, supporting the hypothesis that NO acts as a retrograde messenger during LTP.