Son H, Hawkins R D, Martin K, Kiebler M, Huang P L, Fishman M C, Kandel E R
Howard Hughes Medical Institute and Center for Neurobiology and Behavior, College of Physicians and Surgeons of Columbia University, New York, New York 10032, USA.
Cell. 1996 Dec 13;87(6):1015-23. doi: 10.1016/s0092-8674(00)81796-1.
Nitric oxide (NO) has been implicated in hippocampal long-term potentiation (LTP), but LTP is normal in mice with a targeted mutation in the neuronal form of NO synthase (nNOS-). LTP was also normal in mice with a targeted mutation in endothelial NOS (eNOS-), but LTP in stratum radiatum of CA1 was significantly reduced in doubly mutant mice (nNOS-/eNOS-). By contrast, LTP in stratum oriens was normal in the doubly mutant mice. These results provide the first genetic evidence that NOS is involved in LTP in stratum radiatum and suggest that the neuronal and endothelial forms can compensate for each other in mice with a single mutation. They further suggest that there is also a NOS-independent component of LTP in stratum radiatum and that LTP in stratum oriens is largely NOS independent.
一氧化氮（NO）与海马体长期增强效应（LTP）有关，但在神经元型一氧化氮合酶（nNOS-）发生靶向突变的小鼠中，LTP 是正常的。在内皮型一氧化氮合酶（eNOS-）发生靶向突变的小鼠中，LTP 同样正常，但在双突变小鼠（nNOS-/eNOS-）中，CA1 区辐射层的 LTP 显著降低。相比之下，双突变小鼠中 Oriens 层的 LTP 是正常的。这些结果提供了首个遗传学证据，表明一氧化氮合酶参与辐射层的 LTP，并表明在单突变小鼠中，神经元型和内皮型可以相互补偿。它们进一步表明，辐射层的 LTP 也存在一个不依赖一氧化氮合酶的成分，并且 Oriens 层的 LTP 在很大程度上不依赖一氧化氮合酶。
