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Voltage change-induced gating transitions of the rabbit skeletal muscle Ca2+ release channel

机译:电压变化引起的兔骨骼肌Ca2 +释放通道的门控转换

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摘要

class="enumerated" style="list-style-type:decimal">We used the planar lipid bilayer method to study single ryanodine receptor Ca2+ release channels (RyRCs) from fast skeletal muscle of the rabbit. We found that changes in membrane voltage directly induced gating transitions of the RyRC: (i) in the steady state, even at activating Ca2+ concentrations (20 μm), at a constant membrane potential the channels resided in a low open probability (Po) state (inactivated-, I-mode), and (ii) upon abrupt changes of voltage, the apparent inactivation of the RyRCs was relieved, resulting in a rapid and transient increase in Po.The magnitude of the Po increase was a function of both the duration and the amplitude of the applied prepulse, but was independent of the channel activity during the prepulse.The voltage-induced Po increase probably involved major conformational changes of the channel, as it resulted in substantial alterations in the gating pattern of the channels: the voltage change-induced increase in Po was accompanied by the rapid appearance of two types of channel activity (high (H) and low (L) open probability modes).The response of the RyRC to voltage changes raises the interesting possibility that the activation of RyRC in situ might involve electrical events, i.e. a possible dipole-dipole coupling between the release channel and the voltage sensor.
机译:class =“ enumerated” style =“ list-style-type:decimal”> <!-list-behavior =枚举前缀-word = mark-type = decimal max-label-size = 0-> 我们采用平面脂质双层方法研究了兔快速骨骼肌中单个ryanodine受体Ca 2 + 释放通道(RyRCs)。我们发现,膜电压的变化直接导致RyRC的门控跃迁:(i)在稳态下,即使在激活Ca 2 + 浓度(20μm)时,在恒定的膜电位下,通道也存在在低打开概率(Po)状态(灭活,I模式)下,以及(ii)在电压突然变化时,RyRCs的明显失活得到缓解,导致Po迅速而短暂地增加。 Po升高的幅度是所施加的预脉冲的持续时间和幅度的函数,但与预脉冲期间的通道活动无关。 电压诱导的Po升高可能涉及通道的主要构象变化,因为它导致通道的门控模式发生重大变化:电压变化引起的Po升高伴随着两种类型的通道活性(高(H)和低( L)开放概率模式)。 RyRC t的响应电压变化引起有趣的可能性,即原位RyRC的激活可能涉及电事件,即释放通道和电压传感器之间可能存在偶极-偶极耦合。

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