Hof P R, Pascale E, Magistretti P J
Département de Pharmacologie, Centre Médical Universitaire, Geneva, Switzerland.
J Neurosci. 1988 Jun;8(6):1922-8. doi: 10.1523/JNEUROSCI.08-06-01922.1988.
The effect of increasing [K+]0 on 3H-glycogen levels was examined in mouse cerebral cortical slices. K+ stimulates in a time- and concentration-dependent manner the hydrolysis of 3H-glycogen. Over 70% of the maximal effect is reached within 30 sec and the EC50 for the glycogenolytic action of K+ is 11 mM. Significant 3H-glycogen hydrolysis occurs at 5-12 mM [K+]0, concentrations reached by the ion in the extracellular space during neuronal activity. The K+-evoked glycogenolysis is Ca2+-dependent, and is inhibited by Ca2+-channel blockers such as Ni2+ and Mn2+, but not by Cd2+, nifedipine, and omega-conotoxin. Furthermore, the effect of K+ is not enhanced by the Ca2+-channel agonist Bay K 8644. This type of pharmacological profile suggests that the activation of voltage-sensitive Ca2+ channels of the T subtype mediates the glycogenolytic action of K+. This set of observations suggests that K+ released in the extracellular space by active neurons may promote the mobilization of energy substrates and therefore play a role in the coupling between neuronal activity and energy metabolism.
在小鼠大脑皮质切片中研究了增加细胞外钾离子浓度（[K⁺]₀）对³H-糖原水平的影响。钾离子以时间和浓度依赖性方式刺激³H-糖原的水解。在30秒内可达到最大效应的70%以上，钾离子糖原分解作用的半数有效浓度（EC₅₀）为11 mM。在5 - 12 mM的[K⁺]₀时会发生显著的³H-糖原水解，这是神经元活动期间细胞外空间中该离子所达到的浓度。钾离子诱发的糖原分解是钙依赖性的，并且受到镍离子（Ni²⁺）和锰离子（Mn²⁺）等钙通道阻滞剂的抑制，但不受镉离子（Cd²⁺）、硝苯地平以及ω-芋螺毒素的抑制。此外，钙通道激动剂Bay K 8644不会增强钾离子的作用。这种药理学特征表明，T型电压敏感性钙通道的激活介导了钾离子的糖原分解作用。这一系列观察结果表明，活跃神经元在细胞外空间释放的钾离子可能促进能量底物的动员，因此在神经元活动与能量代谢的偶联中发挥作用。
