Regulatory Mechanisms of Excitability in the Mesencephalic Trigeminal Neurons

（1）MTN神经元中h通道与Na^+-K^+泵之间的双向相互作用h电流（I-h）的激活导致产生两种类型的哇巴因敏感的Na^+-K^+泵电流（I-p），其时间分布与瞬时和慢成分的时间分布相似，推测反映了有限细胞空间中的Na^+瞬变。此外，瞬时I-h激活的I-p可促进慢I-h的后续激活。这些观察结果表明，这种相互作用是双向的，并由Na^+离子介导。同样，在用Li^+取代细胞外Na^+后，尽管I-h本身增强，但尾部I-h显著降低，这是由于I-h的反转电位负移，推测是由于Li^+离子在细胞内积累引起的。这表明存在Na^+微区，在那里可以发生相互作用。与这些发现相一致的是，HCN 1/2亚基和Na^+-K^+泵α3亚型共定位于血浆中 ...更多信息 有许多刺的中脑三叉神经神经元的膜。（2）MT N初级感觉神经元的脉冲传递在索马和轴突丘（AH）的同时膜片钳记录显示，在体细胞去极化过程中存在一个尖峰反向传播，并揭示了尖峰起始位点在干轴突上。在由含QX-314和不含QX-314的贴片移液器产生的从索马到AH的QX-314细胞内浓度梯度降低的条件下，重复电流脉冲注入意外地减弱了AH-尖峰，使索马-尖峰（S-尖峰）几乎不变。当S-或AH-尖峰交替地通过注入电流脉冲到索马或AH和通过刺激干轴突而诱发时，50 nM TTX的浴应用首先使轴突刺激在诱发全或无轴突尖峰中无效，留下S-或AH-尖峰通过注入具有逐步增加的强度的电流脉冲而诱发。在这种条件下，尖峰反向传播不再出现在S-或AH-尖峰。这些观察结果表明，AH和茎轴突上存在低电压激活的、对QX-314和TTX高度敏感的Na^+通道，它们负责棘突反向传播和棘突侵入。此外，取决于S-尖峰是否被反向传播或侵入，类A电流参与了S-尖峰的差异成形，从而以依赖于尖峰起源的方式调节S-尖峰序列的模式。无论是躯体输入还是外周产生的冲动，无论是哪一种，都可能首先在干轴突中触发尖峰，然后被转发到中央轴突，这应该通过索马中形状不同的S-尖峰来反映。少

(1)Bidirectional interactions between h-channels and Na^+-K^+ pumps in MTN neuronsActivation of h-current (I-h) leads to the generation of two types of ouabain-sensitive Na^+-K^+ pump current (I-p) with temporal profiles similar to those of instantaneous and slow components of I-h, presumably reflecting Na^+-transients in a restricted cellular space. Moreover, the I-p activated by instantaneous I-h can facilitate the subsequent activation of slow I-h. These observations indicate that the interactions are bidirectional and mediated by Na^+ ions. Also following substitution of extracellular Na^+ with Li^+, the tail I-h was markedly reduced in spite of an enhancement of I-h itself, due to a negative shift of the reversal potential for I-h presumably caused by intracellular accumulation of Li^+ ions. This suggests the presence of Na^+-microdomain where the interactions can take place. Consistent with these findings, HCN1/2 subunits and the Na^+-K^+ pump α3 isoform were colocalized in plasm … More a membrane of mesencephalic trigeminal neurons having numerous spines.(2)Impulse trafficking in primary sensory neurons of MTNSimultaneous patch-clamp recordings from the soma and axon hillock(AH) revealed a spike-backpropagation in response to somatic depolarization, and disclosed the spike-initiation site in the stem axon. Repetition of current pulse injection, under the condition of decreasing intracellular concentration gradient of QX-314 from the soma to AH created by QX-314-containing and QX-314-free patch pipettes, unexpectedly attenuated the AH-spike, leaving the soma-spike(S-spike) almost unchanged. When S- or AH-spikes were evoked alternately by injection of current pulses into the soma or AH and by stimulation of the stem axon, bath application of 50 nM TTX first rendered the axonal stimulation ineffective in evoking all-or-nothing axonal spikes, leaving the S- or AH-spikes to be evoked by injection of current pulses with a stepwise increased intensity. Under this condition, spike-backpropagation was no longer seen in the S- or AH-spikes. These observations suggest the presence of low-voltage-activated and highly QX-314- and TTX-sensitive Na^+ channels across the AH and stem axon, which are responsible for both spike-backpropagation and spike-invasion. Furthermore, depending on whether S-spikes were backpropagated or invaded, A-like current was involved in differentially shaping S-spikes, thereby regulating the pattern of S-spike trains in a manner dependent on the origin of spikes. It is likely that somatic inputs or peripherally arising impulses whichever trigger spikes in the stem axon first is forwarded to the central axon, which should be reflected by differentially shaped S-spikes in the soma. Less