Regulatory Mechanisms of Excitability in the Mesencephalic Trigeminal Neurons

(1) MTN神经元中h通道和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瓦巴因敏感的Na^+-K^+泵电流（I-p），其时间分布与I-h的瞬时和慢速成分相似，可能反映了Na^+在有限细胞空间中的瞬态。此外，瞬时I-h激活的I-p可以促进后续慢速I-h的激活。这些观察结果表明，相互作用是双向的，并由Na^+离子介导。同样，在细胞外Na^+被Li^+取代之后，尽管I-h本身增强了，但尾I-h却明显减少，这可能是由于Li^+离子在细胞内的积累导致了I-h的逆转电位的负移动。这表明存在Na^+微域，在那里可以发生相互作用。与这些发现一致的是，HCN1/2亚基和Na^+-K^+泵α3亚型共定位于具有多棘的中脑三叉神经元的质膜中。(2) mtn初级感觉神经元的脉冲传输同时来自体细胞和轴突丘（AH）的膜片钳记录显示，在体细胞去极化的响应下，spike-backpropagation（反向传播），并揭示了茎轴突的spike-initiation位点。在含QX-314和不含QX-314的贴片移液器产生的QX-314从体细胞到AH的细胞内浓度梯度降低的情况下，重复电流脉冲注射，出乎意料地减弱了AH峰，使体细胞峰（s峰）几乎保持不变。当通过向体细胞或AH注入电流脉冲和刺激茎轴突交替激发S-或AH-尖峰时，50nm的TTX首先使轴突刺激在激发全或无轴突尖峰方面无效，留下S-或AH-尖峰通过注射逐步增加强度的电流脉冲来激发。在此条件下，S-或ah -棘峰中不再出现棘峰反向传播。这些观察结果表明，在AH和茎轴突上存在低压激活的、QX-314和ttx高度敏感的Na^+通道，这些通道负责尖峰反向传播和尖峰侵袭。此外，取决于s尖峰是否反向传播或入侵，a型电流参与了s尖峰的不同塑造，从而以依赖于尖峰起源的方式调节s尖峰序列的模式。这很可能是躯体输入或周围产生的脉冲，无论哪个触发茎轴突的尖峰，都被转发到中央轴突，这应该通过体细胞中不同形状的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