Maeno T, Hara N, Enomoto K, Ichinose M, Sawada M
Department of Physiology, Shimane Medical University, Izumo, Japan.
Jpn J Physiol. 1995;45(3):397-410. doi: 10.2170/jjphysiol.45.397.
The effect of blockade of ouabain-sensitive alpha 2 and alpha 3 (neural type) isozymes of Na+, K(+)-ATPase was investigated on frog neuromuscular preparations by recording the frequency augmentation-potentiation (FAP) of the endplate potential, an electrophysiological and neuropharmacological technique to analyze the drug actions on the release process of the readily releasable transmitter quanta. Erythrosin B, which was thought to selectively inhibit the neural type Na+, K(+)-ATPase, pivoted the log-linear FAP relation counterclockwise without altering the intercept on the ordinate. Chlormadinone had a similar action. An increase in the concentration of extracellular K+ ions pivoted the FAP relation clockwise with a concomitant upward shift of the intercept on the ordinate, and low K+ Ringer's solution produced an inverse effect. In contrast, Li+ ions shifted the FAP relation upwards dose-dependently leaving its slope unchanged. Cinnarizine, a blocker for inositol-1,4,5-trisphosphate-induced Ca2+ release, and 5,5'-dimethyl-1,2-bis(2-amino-phenoxy)ethane-N,N,N',N'-tetraacetic acid, a specific intracellular Ca2+ chelator, significantly antagonized the potentiating action of Li+. The ouabain-sensitive neural type Na+, K(+)-ATPase isozyme, which is abundant in neural tissues, seems to play an important role in stimulation frequency-dependent modulation of the quantal transmitter release such as FAP.
通过记录终板电位的频率增强-增强作用（FAP），这是一种用于分析药物对易释放递质量子释放过程作用的电生理和神经药理学技术，研究了哇巴因敏感的α2和α3（神经型）Na⁺，K⁺-ATP酶同工酶阻断对青蛙神经肌肉标本的影响。赤藓红B被认为可选择性抑制神经型Na⁺，K⁺-ATP酶，使对数线性FAP关系逆时针旋转，而不改变纵坐标截距。氯地孕酮有类似作用。细胞外K⁺离子浓度增加使FAP关系顺时针旋转，同时纵坐标截距向上移动，而低钾林格液产生相反作用。相反，Li⁺离子使FAP关系剂量依赖性向上移动，斜率不变。桂利嗪是一种肌醇-1,4,5-三磷酸诱导的Ca²⁺释放阻滞剂，5,5'-二甲基-1,2-双（2-氨基苯氧基）乙烷-N,N,N',N'-四乙酸是一种特异性细胞内Ca²⁺螯合剂，它们显著拮抗Li⁺的增强作用。在神经组织中丰富的哇巴因敏感的神经型Na⁺，K⁺-ATP酶同工酶，似乎在诸如FAP等量子递质释放的刺激频率依赖性调节中起重要作用。
