Jiang C, Haddad G G
Department of Pediatrics, Yale University School of Medicine, New Haven, Connecticut 06520, USA.
J Neurophysiol. 1997 Jan;77(1):93-102. doi: 10.1152/jn.1997.77.1.93.
ATP-modulated K+ channels play an important role in regulating membrane excitability during metabolic stress. To characterize such K+ channels from the human brain, single channel currents were studied in excised inside-out patches from freshly dissociated human neocortical neurons. Three currents that were sensitive to physiological concentrations of ATP and selectively permeable to K+ were identified. One of these currents had a unitary conductance of approximately 47 pS and showed a strong inward rectification with symmetric K+ concentrations across the membrane. This K+ current was inhibited by ATP in a concentration-dependent manner with an IC50 (half-inhibition of channel activity) of approximately 130 microM. Channel activity also was suppressed by ADP, non-hydrolyzable ATP analogue AMP-PNP, and sulfonylurea receptor/ channel blocker glibenclamide. The second K+ current had a unitary conductance of approximately 200 pS and showed a weak inward rectification. Similarly, this current was inhibited by ATP (IC50 = 350 microM), AMP-PNP, and glibenclamide. Unlike the small-conductance ATP-inhibitable K+ channel (S-KATP), activation of this large-conductance K+ channel (L-KATP) required the presence of micromolar concentration of Ca2+ in the internal solution, but charybdotoxin did not inhibit this channel. The third K+ current was also Ca2+ dependent and had a large conductance (approximately 280 pS). It was inhibited by external charybdotoxin, iberiotoxin, and tetraethylammonium. In contrast to the other two KATP channels, ATP enhanced channel open-state probability and unitary conductance, and glibenclamide at concentration of 10-20 microM had no inhibitory effect on this current. K+ channels that have single-channel and pharmacological properties similar to these three human ATP-modulated K+ channels also were observed in experiments on rat neocortical neurons. These results therefore indicate that KATP channels are expressed in human neocortical neurons, and two distinct KATP channels (S-KATP and L-KATP) exist in the human and rat neurons. The observation that ATP at different concentrations modulates different K+ channels suggests that metabolic rate may be continuously sensed in neurons with resulting alterations in neuronal membrane excitability.
ATP 调节的钾通道在代谢应激期间调节膜兴奋性方面发挥着重要作用。为了表征来自人类大脑的此类钾通道,我们在新鲜解离的人类新皮质神经元的内向外膜片中研究了单通道电流。鉴定出三种对生理浓度的 ATP 敏感且对 K+ 具有选择性通透性的电流。其中一种电流的单位电导约为 47 pS,在膜两侧 K+ 浓度对称时表现出强烈的内向整流。这种 K+ 电流被 ATP 以浓度依赖性方式抑制,IC50(通道活性的半抑制)约为 130 μM。通道活性也受到 ADP、不可水解的 ATP 类似物 AMP-PNP 和磺脲类受体/通道阻滞剂格列本脲的抑制。第二种 K+ 电流的单位电导约为 200 pS,表现出较弱的内向整流。同样,该电流被 ATP(IC50 = 350 μM)、AMP-PNP 和格列本脲抑制。与小电导 ATP 抑制性钾通道(S-KATP)不同,这种大电导钾通道(L-KATP)的激活需要在内部溶液中存在微摩尔浓度的 Ca2+,但蝎毒素不抑制该通道。第三种 K+ 电流也依赖于 Ca2+,并且具有大电导(约 280 pS)。它被外部蝎毒素、iberiotoxin 和四乙铵抑制。与其他两种 KATP 通道相反,ATP 增加了通道的开放概率和单位电导,并且浓度为 10 - 20 μM 的格列本脲对该电流没有抑制作用。在大鼠新皮质神经元实验中也观察到了具有与这三种人类 ATP 调节的钾通道相似的单通道和药理学特性的钾通道。因此,这些结果表明 KATP 通道在人类新皮质神经元中表达,并且在人类和大鼠神经元中存在两种不同的 KATP 通道(S-KATP 和 L-KATP)。不同浓度的 ATP 调节不同钾通道的观察结果表明,神经元可能持续感知代谢率,从而导致神经元膜兴奋性发生改变。