Bursts of action potential waveforms relieve G-protein inhibition of recombinant P/Q-type Ca2+ channels in HEK 293 cells
Bursts of action potential waveforms relieve G-protein inhibition of recombinant P/Q-type Ca2+ channels in HEK 293 cells
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DOI：
10.1113/jphysiol.1997.sp021956
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发表时间：
1997-03-15
影响因子：
5.5
通讯作者：
Yue, DT
中科院分区：
文献类型：
--
作者：
Brody, DL;Patil, PG;Yue, DT
1.多种神经递质通过G蛋白偶联受体减少突触传递，主要是通过抑制触发神经递质释放的电压门控钙通道。然而，这些突触前钙通道通常无法获得电生理特征。我们利用重组的P/Q型钙通道和M(2)乙酰胆碱受体在HEK 293细胞中重建了这种抑制的一部分。G蛋白抑制钙通道的最有趣的特征之一是强烈的阶跃去极化瞬间解除了这种抑制。我们发现，短脉冲的动作电位电压波形也可以解除这种抑制，增加通过G蛋白抑制的通道的钙电流，而不是通过非抑制的通道。这种缓解的程度随着动作电位波形持续时间的延长而线性增加。这一结果提供了迄今为止最有力的证据，支持G蛋白抑制的缓解可以发生在动作电位的高频序列中。这种效应可能构成了一种新的形式的短期突触可塑性，它对动作电位的时机和持续时间敏感。
1. A variety of neurotransmitters act through G-protein-coupled receptors to decrease synaptic transmission, largely by inhibiting the voltage-gated calcium channels that trigger neurotransmitter release. However, these presynaptic calcium channels are typically inaccessible to electrophysiological characterization. We have reconstituted a part of this inhibition using recombinant P/Q-type calcium channels and M(2) acetylcholine receptors in HEK 293 cells.2. One of the most interesting features of G-protein inhibition of calcium channels is that strong step depolarization transiently relieves the inhibition. We have found that short bursts of action potential voltage waveforms can also relieve the inhibition, increasing calcium current through G-protein-inhibited channels but not through uninhibited channels.3. The extent of this relief increased linearly with the duration of the action potential waveforms.4. This result provides the strongest evidence to date favouring the possibility that relief of G-protein inhibition can occur during high frequency trains of action potentials. This effect may constitute a novel form of short-term synaptic plasticity that is sensitive to action potential timing and duration.