Kuba K, Nishi S
J Neurophysiol. 1976 May;39(3):547-63. doi: 10.1152/jn.1976.39.3.547.
Superfusion of the isolated sympathetic ganglion of the bullfrog with a caffeine-containing (1-6 mM) solution caused in many cells an initial slow hyperpolarization which was followed by a subliminal depolarization interruped by rhythmic hyperpolarizations. A hyperpolarization, similar to one of the rhythmic hyperpolarizations, could be triggered by an action potential in the presence of caffeine. The action potential itself was not markedly affected by caffeine except for its afterhyperpolarization which was prolonged. All these caffeine-induced hyperpolarizations were associated with a marked reduction of the membrane resistance, their amplitude was increased in a K+-free solution and decreased in a high-K+ solution, and their polarity was reversed at the same level at which the afterhyperpolarization was also inverted. This reversal level was not altered by omission of Na+ or C1- from the external medium. These hyperpolarizations were reversibly abolished by depletion of external Ca2+ or replacement of external Ca2+ by Mg2+. Excess of external Ca2+ caused a shortening of the interval between rhythmic hyperpolarizations. Furthermore, iontophoretic injection of EDTA into the cytoplasm markedly depressed the initial caffeine hyperpolarizatin and abolished both the rhythmic and evoked caffeine hyperpolarizations. The caffeine-induced depolarization was not affected by omission of external Cl-. It was decreased in a Na+-free medium, but completely eliminated by omission of both Na+ and Ca2+ from the external medium. Tetrodotoxin did not impair the production of the initial and the rhythmic hyperpolarizations. A strong depolarizing pulse could evoke a typical hyperpolarizing response in the presence of this compound. Dibutyryl cyclic AMP, d-tubocurarine, atropine, and phenoxybenzamine were without effect on the caffeine-induced hyperpolarizations and depolarization. It was concluded that each caffeine-induced hyperpolarization is the result of an increased K+ permeability, which is probably caused by a rise in the internal Ca2+ concentration. It was also concluded that the caffeine-induced depolarization is due to an increased membrane permeability to Ca2+ and Na+.
用含咖啡因（1 - 6 mM）的溶液对牛蛙离体交感神经节进行灌流，在许多细胞中引发了初始的缓慢超极化，随后是阈下去极化，并被节律性超极化打断。在咖啡因存在的情况下，动作电位可引发类似于节律性超极化之一的超极化。动作电位本身除了后超极化延长外，未受到咖啡因的明显影响。所有这些咖啡因诱导的超极化都与膜电阻的显著降低相关，其幅度在无钾溶液中增加，在高钾溶液中降低，并且其极性在与后超极化反转相同的水平上反转。这种反转水平不受外部介质中钠或氯缺失的影响。这些超极化可通过耗尽外部钙离子或用镁替代外部钙离子而可逆地消除。过量的外部钙离子导致节律性超极化之间的间隔缩短。此外，向细胞质中离子电泳注射乙二胺四乙酸（EDTA）显著抑制了初始的咖啡因超极化，并消除了节律性和诱发的咖啡因超极化。咖啡因诱导的去极化不受外部氯缺失的影响。在无钠介质中它降低，但通过从外部介质中同时去除钠和钙而完全消除。河豚毒素不损害初始和节律性超极化的产生。在这种化合物存在的情况下，强去极化脉冲可引发典型的超极化反应。二丁酰环磷腺苷、d - 筒箭毒碱、阿托品和酚苄明对咖啡因诱导的超极化和去极化均无影响。得出的结论是，每个咖啡因诱导的超极化是钾通透性增加的结果，这可能是由于细胞内钙浓度升高所致。还得出结论，咖啡因诱导的去极化是由于膜对钙和钠的通透性增加。
