Ewald D, Eckert R
Cell Mol Neurobiol. 1983 Dec;3(4):345-53. doi: 10.1007/BF00734715.
The effect on the Ca-dependent potassium current, IK(Ca), of procedures that increase intracellular cAMP levels was studied in Aplysia neurons using three different pharmacological approaches. Exposure to cAMP analogues which were either resistant to or protected from phosphodiesterase hydrolysis caused an increase in IK(Ca) from 30 to 50% in 10 min. The degree of reversibility of this effect varied from complete with db cAMP to very little with pcpt cAMP. Exposure to cholera toxin, which stimulates the synthesis of endogenous cAMP, increased IK(Ca) 25% in 10 min and the effect was not reversible. Both approaches were effective in all seven neuron types studied. Application of serotonin plus phosphodiesterase inhibitor caused an increase in IK(Ca) in neuron R15 but not in the other neuron types. Application of pentylene tetrazole (PTZ) led to a decrease in IK(Ca). It is proposed that elevation of cyclic AMP mediates an increased sensitivity of the IK(Ca) channel to Ca ions.
运用三种不同的药理学方法,在海兔神经元中研究了提高细胞内cAMP水平的操作对钙依赖性钾电流(IK(Ca))的影响。暴露于对磷酸二酯酶水解具有抗性或受到保护的cAMP类似物中,10分钟内IK(Ca)增加了30%至50%。这种效应的可逆程度有所不同,从与二丁酰环磷腺苷完全可逆到与对氯苯硫磷酰环磷腺苷几乎不可逆。暴露于刺激内源性cAMP合成的霍乱毒素中,10分钟内IK(Ca)增加了25%,且该效应不可逆。这两种方法在所有研究的七种神经元类型中均有效。血清素加磷酸二酯酶抑制剂的应用使R15神经元中的IK(Ca)增加,但在其他神经元类型中未增加。戊四氮(PTZ)的应用导致IK(Ca)降低。有人提出,环磷酸腺苷的升高介导了IK(Ca)通道对钙离子的敏感性增加。