Cohen A S, Weinreich D, Kao J P
Department of Pharmacology and Experimental Therapeutics, University of Maryland School of Medicine, Baltimore 21201-1559.
Neurosci Lett. 1994 May 23;173(1-2):17-20. doi: 10.1016/0304-3940(94)90140-6.
A Ca(2+)-dependent slow spike after hyperpolarization (AHPslow) is present in about 35% of the neurons in the nodose ganglion. Although the AHPslow profoundly affects spike frequency accommodation of these neurons, the mechanisms that control the generation and the duration of the AHPslow are unclarified. N omega-Nitro-L-arginine methyl ester (L-NAME; 10 microM), a specific inhibitor of nitric oxide synthase (NOS), reduced the AHPslow by more than 92%. The L-NAME block of the AHPslow was antagonized by application of 50 microM S-nitroso-N-acetylpenicillamine (SNAP), a nitric oxide donor. The fast, Ca(2+)-dependent, spike after hyperpolarization preceding the AHPslow and the elevation of intracellular Ca2+ accompanying the AHPslow were unaffected by L-NAME treatment. These findings indicate that products of NOS activity might directly or indirectly activate the AHPslow K+ channels at a step beyond Ca2+ influx or intracellular Ca2+ mobilization.
在结状神经节中，约35%的神经元存在一种超极化后钙依赖的慢电位（AHPslow）。尽管AHPslow深刻影响这些神经元的放电频率适应性，但控制AHPslow产生和持续时间的机制尚不清楚。一氧化氮合酶（NOS）的特异性抑制剂Nω-硝基-L-精氨酸甲酯（L-NAME；10微摩尔）使AHPslow降低了92%以上。AHPslow的L-NAME阻断作用可被一氧化氮供体50微摩尔S-亚硝基-N-乙酰青霉胺（SNAP）的应用所拮抗。在AHPslow之前的快速、钙依赖的超极化后电位以及伴随AHPslow的细胞内Ca2+升高不受L-NAME处理的影响。这些发现表明，NOS活性产物可能在Ca2+内流或细胞内Ca2+动员之外的步骤直接或间接激活AHPslow钾通道。
