Contribution of outward currents to spike-frequency adaptation in hypoglossal motoneurons of the rat.
Contribution of outward currents to spike-frequency adaptation in hypoglossal motoneurons of the rat.
复制标题
外向电流对大鼠舌下运动神经元尖峰频率适应的贡献。
DOI：
10.1152/jn.1997.78.5.2246
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发表时间：
1997
期刊：
影响因子：
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通讯作者：
Binder,MD
中科院分区：
文献类型：
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作者：
Sawczuk,A;Powers,RK;Binder,MD
放大图片作者：Andrea K. Powers和Marc D. Binder.大鼠舌下神经运动神经元外向电流对尖峰频率适应的贡献。神经生理学杂志78：2246-2253，1997。尖峰频率适应已被归因于几种不同的膜电流的作用。在这项研究中，我们评估的贡献，这些电流：净外向电流所产生的产电Na+-K+泵和外向电流，流经Ca 2+激活的K+通道。在对大鼠脑干切片的舌下神经运动神经元进行记录时，我们发现，水浴应用4-20 μM哇巴因溶液可部分阻断Na ~+-K ~+泵的活性，这一点可由持续放电一段时间后的放电后超极化显著降低所证明。然而，我们没有观察到显着的变化，无论是在初始，早期，或后期阶段的尖峰频率适应哇巴因的存在。适应也与增加的持续时间和幅度的中期后超极化（mAHP）介导的钙激活的K+通道。当我们用Mn 2+替换浴液中的2 mM Ca 2+时，尖峰后mAHP的振幅显著降低。mAHP幅度的减少导致尖峰频率适应的初始阶段的幅度减少，正如其他人以前所报道的那样。然而，出乎意料的是，我们还发现，降低mAHP导致适应的早期和晚期阶段的幅度急剧增加。这些变化可以通过恢复浴中正常的Ca 2+浓度来逆转。我们的研究结果与哇巴因表明，Na+-K+泵在大鼠舌下神经运动神经元的适应的三个阶段中发挥的作用很小，如果有的话。我们的研究结果与Ca 2+通道阻断支持的假设，即初始适应，部分，控制电导的mAHP。然而，我们未能通过阻断Ca 2+通道完全消除初始适应，这表明其他膜机制也有贡献。最后，在存在Mn 2+阻断Ca 2+通道的情况下，适应的早期和晚期都增加，这进一步支持了以下假设：尖峰频率适应的早期和晚期）阶段由不同的细胞机制介导。
Sawczuk, Andrea, Randall K. Powers, and Marc D. Binder.Contribution of outward currents to spike-frequency adaptation in hypoglossal motoneurons of the rat.J. Neurophysiol.78: 2246–2253, 1997. Spike-frequency adaptation has been attributed to the actions of several different membrane currents. In this study, we assess the contributions of two of these currents: the net outward current generated by the electrogenic Na+-K+pump and the outward current that flows through Ca2+-activated K+channels. In recordings made from hypoglossal motoneurons in slices of rat brain stem, we found that bath application of a 4–20 μM ouabain solution produced a partial block of Na+-K+pump activity as evidenced by a marked reduction in the postdischarge hyperpolarization that follows a period of sustained discharge. However, we observed no significant change in either the initial, early, or late phases of spike-frequency adaptation in the presence of ouabain. Adaptation also has been related to increases in the duration and magnitude of the medium-duration afterhyperpolarization (mAHP) mediated by Ca2+-activated K+channels. When we replaced the 2 mM Ca2+in the bathing solution with Mn2+, there was a significant decrease in the amplitude of the mAHP after a spike. The decrease in mAHP amplitude resulted in a decrease in the magnitude of the initial phase of spike-frequency adaptation as has been reported previously by others. However, quite unexpectedly we also found that reducing the mAHP resulted in a dramatic increase in the magnitude of both the early and late phases of adaptation. These changes could be reversed by restoring the normal Ca2+concentration in the bath. Our results with ouabain indicate that the Na+-K+pump plays little, if any, role in the three phases of adaptation in rat hypoglossal motoneurons. Our results with Ca2+channel blockade support the hypothesis that initial adaptation is, in part, controlled by conductances underlying the mAHP. However, our failure to eliminate initial adaptation completely by blocking Ca2+channels suggests that other membrane mechanisms also contribute. Finally, the increase in both the early and late phases of adaptation in the presence of Mn2+block of Ca2+channels lends further support to the hypothesis that the initial and later (i.e., early and late) phases of spike-frequency adaptation are mediated by different cellular mechanisms.