长时程增强
一氧化氮合酶
生物
伊诺斯
突变体
内皮一氧化氮合酶
海马结构
一氧化氮
一氧化氮合酶Ⅲ型
细胞生物学
神经科学
内分泌学
生物化学
基因
受体
作者
Hyeon Son,Robert D. Hawkins,Kelsey C. Martin,Michael Kiebler,Paul L. Huang,Mark C. Fishman,Eric R. Kandel
出处
期刊:Cell
[Elsevier]
日期:1996-12-01
卷期号:87 (6): 1015-1023
被引量:421
标识
DOI:10.1016/s0092-8674(00)81796-1
摘要
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.
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