Arancio O, Kiebler M, Lee C J, Lev-Ram V, Tsien R Y, Kandel E R, Hawkins R D
Center for Neurobiology and Behavior, College of Physicians and Surgeons, Columbia University, New York, New York 10032, USA.
Cell. 1996 Dec 13;87(6):1025-35. doi: 10.1016/s0092-8674(00)81797-3.
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 scavenger, 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.
一氧化氮（NO）被认为在海马体CA1区的长时程增强（LTP）过程中作为逆行信使发挥作用，但突触前终末难以接近阻碍了对这一假设的确定性检验。由于在培养的海马神经元中突触两侧均可接近，我们利用这种制备方法来研究NO的作用。我们在细胞内或细胞外应用NO清除剂、NO合酶抑制剂以及仅在紫外光照射下才释放NO的膜不通透性NO供体后检测LTP。我们的结果表明，NO在突触后神经元中产生，穿过细胞外空间，并直接作用于突触前神经元以产生长时程增强，支持了NO在LTP过程中作为逆行信使发挥作用的假设。
