Calcium conductances and their role in the firing behavior of neonatal rat hypoglossal motoneurons.
Calcium conductances and their role in the firing behavior of neonatal rat hypoglossal motoneurons.
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钙电导及其在新生大鼠舌下运动神经元放电行为中的作用。
DOI：
10.1152/jn.1993.69.6.2137
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发表时间：
1993
影响因子：
2.5
通讯作者：
Berger,AJ
中科院分区：
文献类型：
--
作者：
Viana,F;Bayliss,DA;Berger,AJ
1.采用细胞内记录和膜片钳技术，在新生大鼠（0-15日龄）脑片上研究了舌下神经运动神经元（HMs）的钙电导在动作电位产生和重复放电行为中的作用。2.动作电位之后是后去极化（ADP）。ADP呈电压依赖性，随膜超极化而增加。提高细胞外Ca ~（2+）浓度或以Ba ~（2+）替代Ca ~（2+）可使ADP幅值增加，而以Mn ~（2+）替代Ca ~（2+）则可使ADP幅值降低，阿米洛利和低浓度Ni ~（2+）可使ADP幅值降低。3.个别新生HM的放电行为受到膜电位的影响。从去极化电位，HMs发射强直性响应于去极化电流脉冲，而从更多的超极化膜电位（比-70 mV更负），一个子集的HMs发射了一个初始的动作电位爆发，随后是一个长期的后超极化和强直性放电。爆发放电行为的发生率在年轻的运动神经元中最高，并在出生后第10天消失。此外，突出的反弹去极化的特点是新生儿运动神经元的反应超极化前脉冲。4.反跳去极化的药理学表征表明它是钙依赖性的。其振幅对河豚毒素不敏感，用Mn ~（2+）替代Ca ~（2+）或加入Ni ~（2+）可使其消失。阿米洛利（1-1.5 mM）对反弹反应或爆发性放电没有影响。5.高阈值钙峰的存在下，检测在所有出生后的年龄，但只有在封锁外向电流与内部或细胞外四乙铵。当Ba ~（2+）替代Ca ~（2+）时，高阈值钙峰显著增强。6.钙电流的新生儿HM的特点是在全细胞膜片钳记录薄髓片的条件下，最大限度地减少电压依赖性Na+和K+电流。低电压激活（LVA）和高电压激活（HVA）的钙电流成分的基础上，他们的电压阈值激活，失活动力学，和药理学敏感性。7. LVA钙电流在-60 mV左右开始激活，并在100 ms内几乎完全失活。完全稳态失活发生在电位大于-60 mV时。1 mM阿米洛利可选择性地降低LVA电流（31%）。8.在-35 mV左右的电位下激活较大幅度的钙电流。这种HVA电流的失活比LVA电流的失活慢并且不完全。该电流的约1/3对1 μ M ω-芋螺毒素GVIA敏感，而较小部分被10 μ M硝苯地平阻断。（400字处截断摘要）
1. The role of calcium conductances in action potential generation and repetitive firing behavior of hypoglossal motoneurons (HMs) was investigated using intracellular recording and patch-clamp techniques in a brain stem slice preparation of neonatal rats (0-15 days old). 2. The action potential was followed by an afterdepolarization (ADP). The ADP was voltage dependent, increasing with membrane hyperpolarization. Raising the extracellular Ca2+ concentration or replacing Ca2+ with Ba2+ increased the ADP amplitude, whereas replacement of Ca2+ with Mn2+ blocked it. The ADP was partially reduced by amiloride and low concentrations of Ni2+. 3. The firing behavior of individual neonatal HMs was influenced by membrane potential. From depolarized potentials, HMs fired tonically in response to a depolarizing current pulse, whereas from more hyperpolarized membrane potentials (more negative than -70 mV), a subset of HMs fired an initial burst of action potentials followed by a prolonged afterhyperpolarization and tonic firing. The incidence of burst-firing behavior was highest among young motoneurons and disappeared by the tenth postnatal day. In addition, prominent rebound depolarizations characterized the response of neonatal motoneurons to hyperpolarizing prepulses. 4. Pharmacological characterization of the rebound depolarization demonstrated that it was calcium dependent. Its amplitude was insensitive to tetrodotoxin and it was eliminated by replacement of Ca2+ with Mn2+ or addition of Ni2+. Amiloride (1-1.5 mM) had no effect on the rebound response or burst firing. 5. The presence of high-threshold calcium spikes was detected at all postnatal ages, but only after blockade of outward currents with intra- or extracellular tetraethylammonium. The high-threshold calcium spikes were greatly enhanced when Ba2+ replaced Ca2+. 6. Calcium currents of neonatal HMs were characterized in whole-cell patch-clamp recordings of thin medullary slices under conditions that minimized voltage-dependent Na+ and K+ currents. Low voltage-activated (LVA) and a high voltage-activated (HVA) calcium current components were identified on the basis of their voltage thresholds for activation, kinetics of inactivation, and pharmacological sensitivity. 7. The LVA calcium current began to activate at around -60 mV and inactivated nearly completely within 100 ms. Complete steady-state inactivation occurred at potentials more positive than -60 mV. The LVA current was selectively reduced by 1 mM amiloride (31%). 8. A larger-amplitude calcium current activated at potentials around -35 mV. Inactivation of this HVA current was slower than that of the LVA current and incomplete. About 1/3 of this current was sensitive to 1 microM omega-conotoxin GVIA, whereas a smaller fraction was blocked by 10 microM nifedipine.(ABSTRACT TRUNCATED AT 400 WORDS)
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