Haley J E, Wilcox G L, Chapman P F
Department of Psychology, University of Minnesota, Minneapolis 55455.
Neuron. 1992 Feb;8(2):211-6. doi: 10.1016/0896-6273(92)90288-o.
Long-term potentiation is a long-lasting, use-dependent increase in the strength of synaptic connections. We investigated the role of nitric oxide (NO) in determining the duration of potentiation induced by high frequency stimulation of afferents in the CA1 region of the rat hippocampus. The calcium/calmodulin-dependent production of NO can be initiated by activation of excitatory amino acid receptors and results in increased levels of cGMP in target cells. Here we report that only a relatively short-term potentiation can be induced in the presence of nitro-L-arginine methyl ester (L-NAME), an NO synthase inhibitor. The effects of L-NAME on the duration of potentiation are partially reversed by coadministration of L-arginine, a precursor of neuronal NO, and by dibutyryl cGMP. Hemoglobin, which binds extracellular NO, also shortens the duration of stimulus-induced potentiation. The results suggest a role for NO in the maintenance of activity-dependent synaptic enhancements, possibly via the generation of cGMP.
长时程增强是突触连接强度的一种持久的、依赖使用的增加。我们研究了一氧化氮（NO）在决定大鼠海马体CA1区传入纤维高频刺激诱导的增强持续时间中的作用。NO的钙/钙调蛋白依赖性产生可由兴奋性氨基酸受体的激活引发，并导致靶细胞中cGMP水平升高。在此我们报告，在一氧化氮合酶抑制剂硝基-L-精氨酸甲酯（L-NAME）存在的情况下，只能诱导出相对短期的增强。L-精氨酸（神经元NO的前体）和二丁酰cGMP的共同给药可部分逆转L-NAME对增强持续时间的影响。结合细胞外NO的血红蛋白也会缩短刺激诱导的增强持续时间。结果表明NO可能通过生成cGMP在维持活动依赖性突触增强中发挥作用。
