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体外研究大鼠新生运动神经元放电特性的离子机制。

Ionic mechanisms underlying the firing properties of rat neonatal motoneurons studied in vitro.

作者信息

Walton K, Fulton B P

出版信息

Neuroscience. 1986 Nov;19(3):669-83. doi: 10.1016/0306-4522(86)90291-5.

Abstract

Ionic mechanisms underlying the firing properties of spinal motoneurons of neonatal rats (postnatal days 3-10) have been investigated using a hemisected, in vitro spinal cord preparation. These results demonstrate the presence of a high-threshold voltage-dependent calcium response and partial sodium-dependent spikes. The calcium current is evident during the falling phase of the action potential and is the major component of the after-depolarizing potential. The subsequent increase in intracellular calcium concentration activates a calcium-dependent potassium conductance (gK-Ca), the major component of the after-hyperpolarizing potential. The gCa, by activating gK-Ca, is the primary determinant of firing rate in neonatal motoneurons. For, when gCa was blocked by Cd2+, the interspike interval decreased, the maximum firing rate and the slope of the firing frequency-injected current relation increased. The calcium current is particularly robust during the first few postnatal days; during this period, tetrodotoxin resistant action potentials can be elicited by direct stimulation under control conditions. In animals older than 5 days such calcium spikes could be elicited only after decreasing gK with intracellular Cs+ or extracellular tetraethylammonium. This was the case even when 1 mM of the bath CaCl2 was replaced with BaCl2. The rising phases of calcium spikes recorded from neurons in both age groups demonstrate several components suggesting the calcium spikes comprise several discrete events, which probably originate across the dendritic membrane. When gK was decreased by bath application of tetraethylammonium+ and Cs+, neonatal motoneurons generated prolonged Ca-dependent spikes lasting for up to 6 s. Repolarization of Ca spikes occurred in two stages, the first was rapid (-2.11 +/- 0.8 V/s, n = 6) but incomplete. The second, was slower (-0.01 +/- 0.003 V/s, n = 5) and returned the membrane potential to the resting level after about 1-2 s. It is suggested that accumulation of extracellular potassium may contribute to the slow phase of repolarization. Motoneurons from the younger age group (3-5 days old) demonstrate all-or-none partial spikes rising from the after-depolarization of directly elicited sodium-dependent action potentials. Similar partial spikes were elicited from neurons from older animals during intracellular Cs+ loading. The partial spikes had faster rates of rise than the tetrodotoxin-resistant spikes and were not seen after tetrodotoxin treatment, suggesting that they are sodium-dependent.(ABSTRACT TRUNCATED AT 400 WORDS)

摘要

利用半切的体外脊髓标本,对新生大鼠(出生后3 - 10天)脊髓运动神经元放电特性的离子机制进行了研究。这些结果表明存在高阈值电压依赖性钙反应和部分钠依赖性动作电位。钙电流在动作电位的下降阶段明显,是去极化后电位的主要成分。随后细胞内钙浓度的增加激活了钙依赖性钾电导(gK-Ca),这是超极化后电位的主要成分。gCa通过激活gK-Ca,是新生运动神经元放电频率的主要决定因素。因为,当gCa被Cd2+阻断时,峰间期缩短,最大放电频率以及放电频率-注入电流关系的斜率增加。钙电流在出生后的头几天特别强劲;在此期间,在对照条件下直接刺激可诱发对河豚毒素有抗性的动作电位。在5日龄以上的动物中,只有在用细胞内Cs+或细胞外四乙铵降低gK后才能诱发这种钙动作电位。即使将浴槽中的1 mM CaCl2替换为BaCl2,情况也是如此。两个年龄组神经元记录到的钙动作电位的上升阶段显示出几个成分,表明钙动作电位由几个离散事件组成,这些事件可能起源于树突膜。当通过浴槽应用四乙铵和Cs+降低gK时,新生运动神经元产生持续长达6秒的延长的钙依赖性动作电位。钙动作电位的复极化分两个阶段进行,第一阶段很快(-2.11±0.8 V/s,n = 6)但不完全。第二阶段较慢(-0.01±0.003 V/s,n = 5),并在约1 - 2秒后将膜电位恢复到静息水平。提示细胞外钾的积累可能有助于复极化的慢相。较年轻年龄组(3 - 5日龄)的运动神经元表现出全或无的部分动作电位,这些动作电位由直接诱发的钠依赖性动作电位的去极化后电位产生。在细胞内加载Cs+期间,较年长动物的神经元也诱发了类似的部分动作电位。这些部分动作电位的上升速度比河豚毒素抗性动作电位快,并且在河豚毒素处理后未见,表明它们是钠依赖性的。(摘要截短于400字)

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