电活动和胞质钙调节培养的大鼠肌肉细胞中对河豚毒素敏感的钠通道水平。
Electrical activity and cytosolic calcium regulate levels of tetrodotoxin-sensitive sodium channels in cultured rat muscle cells.
作者信息
Sherman S J, Catterall W A
出版信息
Proc Natl Acad Sci U S A. 1984 Jan;81(1):262-6. doi: 10.1073/pnas.81.1.262.
Abstract
Pharmacological blockade of the spontaneous electrical activity present in primary cultures of rat myotubes by growth in bupivacaine, tetrodotoxin, or KCl was found to increase the number of voltage-sensitive Na+ channels 38-83% as measured by the specific binding of [3H]saxitoxin. The inhibition of spontaneous electrical activity and increase in channel density by bupivacaine displayed an identical dose response, with a half-maximal effect at 3.0 microM. Growth of myotubes in the presence of 1 microM A23187, a Ca2+-specific ionophore, resulted in a 30-60% decrease in the number of tetrodotoxin-sensitive channels with no change in affinity for [3H]saxitoxin. A23187 was able to overcome the increase in channel density produced by bupivacaine. These results suggest the presence of a Ca2+-mediated negative feedback system in which electrical excitability may be regulated by altering the number of tetrodotoxin-sensitive Na+ channels.
摘要
通过在布比卡因、河豚毒素或氯化钾中培养，发现大鼠肌管原代培养物中存在的自发电活动的药理学阻断可使电压敏感性钠通道数量增加38 - 83%，这是通过[3H]石房蛤毒素的特异性结合来测量的。布比卡因对自发电活动的抑制和通道密度的增加呈现相同的剂量反应，在3.0微摩尔时达到最大效应的一半。在1微摩尔A23187（一种Ca2+特异性离子载体）存在下培养肌管，导致河豚毒素敏感性通道数量减少30 - 60%，而对[3H]石房蛤毒素的亲和力没有变化。A23187能够克服布比卡因引起的通道密度增加。这些结果表明存在一种Ca2+介导的负反馈系统，其中电兴奋性可能通过改变河豚毒素敏感性钠通道的数量来调节。
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