Henquin J C, Meissner H P
J Physiol. 1984 Jun;351:595-612. doi: 10.1113/jphysiol.1984.sp015265.
The effects of theophylline and dibutyryl cyclic AMP on the membrane potential of mouse beta-cells were studied with micro-electrodes. They were compared to their effects on insulin release by perifused mouse islets. In 3 mM-glucose, theophylline (10 mM) depolarized the beta-cell membrane and stimulated insulin release, but did not induce electrical activity. Dibutyryl cyclic AMP (1 mM) was without effect. In 7 mM-glucose, theophylline (0.5-2 mM) and dibutyryl cyclic AMP (1 mM) slightly depolarized the beta-cell membrane, induced electrical activity in otherwise silent cells and increased insulin release. A higher concentration of theophylline (10 mM) hyperpolarized the beta-cell membrane, did not induce electrical activity, but also stimulated insulin release. In 10 mM-glucose, the membrane potential of beta-cells exhibited repetitive slow waves with bursts of spikes on the plateau. Under steady state, these slow waves were differently affected by low or high concentrations of theophylline. At 0.5-2 mM, theophylline shortened the intervals, lengthened the slow waves and slightly increased their frequency. On the other hand, 10 mM-theophylline markedly decreased the duration of both intervals and slow waves, and increased their frequency. The effects of 1 mM-dibutyryl cyclic AMP were similar to those of 2 mM-theophylline. With 2-10 mM-theophylline, two other effects were also observed: a transient hyperpolarization with suppression of electrical activity immediately after addition of the methylxanthine and an increase in electrical activity upon its withdrawal. Theophylline and dibutyryl cyclic AMP markedly potentiated insulin release induced by 10 mM-glucose. The magnitude of these changes did not correlate well with the importance of the changes in electrical activity. However, with 2-10 mM-theophylline the increase in release was also preceded by an initial transient inhibition, whereas withdrawal of the methylxanthine was accompanied by a further increase. When Ca influx was inhibited by D600, the slow waves were suppressed, the membrane was depolarized to the plateau level and only few spikes were present. Although theophylline markedly increased insulin release under these conditions, it did not affect the membrane potential. Several conclusions can be drawn from this study. Insulin release and electrical activity in beta-cells can be dissociated when intracellular Ca is used to trigger exocytosis. High concentrations of theophylline produce effects unrelated to cyclic AMP.(ABSTRACT TRUNCATED AT 400 WORDS)
采用微电极研究了茶碱和二丁酰环磷腺苷(dibutyryl cyclic AMP)对小鼠β细胞静息膜电位的影响,并将其与它们对灌流小鼠胰岛胰岛素释放的影响进行了比较。在3 mM葡萄糖环境中,茶碱(10 mM)使β细胞膜去极化并刺激胰岛素释放,但未诱发电活动。二丁酰环磷腺苷(1 mM)则无此作用。在7 mM葡萄糖环境中,茶碱(0.5 - 2 mM)和二丁酰环磷腺苷(1 mM)使β细胞膜轻度去极化,在原本静息的细胞中诱发电活动,并增加胰岛素释放。较高浓度的茶碱(10 mM)使β细胞膜超极化,未诱发电活动,但也刺激胰岛素释放。在10 mM葡萄糖环境中,β细胞的膜电位呈现重复性慢波,在平台期有峰电位爆发。在稳态下,这些慢波受到低浓度或高浓度茶碱的不同影响。在0.5 - 2 mM时,茶碱缩短了间隔时间,延长了慢波,并略微增加了其频率。另一方面,10 mM茶碱显著缩短了间隔时间和慢波的持续时间,并增加了其频率。1 mM二丁酰环磷腺苷的作用与2 mM茶碱相似。使用2 - 10 mM茶碱时,还观察到另外两种效应:加入甲基黄嘌呤后立即出现短暂超极化并抑制电活动,撤药后电活动增加。茶碱和二丁酰环磷腺苷显著增强了10 mM葡萄糖诱导的胰岛素释放。这些变化的幅度与电活动变化的程度相关性不佳。然而,使用2 - 10 mM茶碱时,释放增加之前也有初始短暂抑制,而撤去甲基黄嘌呤后则伴随进一步增加。当用D600抑制钙内流时,慢波被抑制,膜去极化至平台水平,仅出现少数峰电位。尽管在这些条件下茶碱显著增加胰岛素释放,但它不影响膜电位。从本研究可得出几个结论。当细胞内钙用于触发胞吐作用时,β细胞中的胰岛素释放和电活动可以分离。高浓度茶碱产生的效应与环磷腺苷无关。