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正常和营养不良小鼠脊髓运动神经元的电生理特性

Electrophysiological properties of spinal motoneurones of normal and dystrophic mice.

作者信息

Huizar P, Kuno M, Miyata Y

出版信息

J Physiol. 1975 Jun;248(1):231-46. doi: 10.1113/jphysiol.1975.sp010971.

DOI:10.1113/jphysiol.1975.sp010971
PMID:168358
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1309516/
Abstract
  1. The properties of spinal motoneurones of normal and dystrophic mice (129/ReJ) were examined with intracellular electrodes. 2. The following parameters of spinal motoneurones showed no significant differences between normal and dystrophic mice: resting and action potentials, the amplitude and duration of after-hyperpolarization, rheobasic current for excitation, threshold for excitation of the somadendritic membrane (IS-SD inflexion) and input resistance. 3. The changes in motoneurone properties observed 13-16 days after section of the sciatic nerve (axotomy) were similar in both normal and dystrophic mice. 4. The axonal conduction velocity of motoneurones in dystrophic mice was about ten times slower than that in normal mice. The conduction velocity of the sciatic nerve was only about 25% slower in dystrophic mice than in the normal animal. The estimated ventral root conduction velocity as well as the observed dorsal root conduction velocity in dystrophic mice was at least twenty times slower than that in normal mice. 5. In dystrophic mice, spinal motoneurones often showed multiple discharges in response to single, antidromic stimuli. The site of initiation of multiple discharge was located in the motor axon rather than in the motoneurone cell body. 6. In dystrophic mice, nerve impulses were transmitted from fibre to fibre ('cross-talk'). The site of impulse transmission among nerve fibres was near the distal portion of the spinal roots. 7. Synaptic potentials and peripheral reflex discharges evoked by stimulation of the dorsal roots showed a longer latency and were more prolonged in dystrophic mice than in the control mice. 8. The motoneurone properties of dystrophic mice showed no tendency of progressive changes with age ranging from 63 to 148 days. 9. It is concluded that the properties of motoneurone cell bodies examined in dystrophic mice are indistinguishable from those in normal mice and that the only abnormality in motoneurones of the former residues in the motor axon. 10. It is suggested that integrity of the discharge pattern of spinal motoneurones in dystrophic mice is interfered by anomalous impluse transmission in the motor axons and that the motoneurones in dystrophic mice are a homogeneous group rather than a mixture of "normal" and "abnormal" neurones.
摘要
  1. 用细胞内电极检测正常和营养不良小鼠(129/ReJ)脊髓运动神经元的特性。2. 脊髓运动神经元的以下参数在正常和营养不良小鼠之间无显著差异:静息电位和动作电位、超极化后电位的幅度和持续时间、兴奋的基强度电流、胞体树突膜兴奋阈值(IS-SD 拐点)和输入电阻。3. 在坐骨神经切断(轴突切断)13 - 16 天后观察到的运动神经元特性变化在正常和营养不良小鼠中相似。4. 营养不良小鼠运动神经元的轴突传导速度比正常小鼠慢约 10 倍。营养不良小鼠坐骨神经的传导速度仅比正常动物慢约 25%。营养不良小鼠估计的腹根传导速度以及观察到的背根传导速度至少比正常小鼠慢 20 倍。5. 在营养不良小鼠中,脊髓运动神经元常对单个逆向刺激表现出多次放电。多次放电的起始部位位于运动轴突而非运动神经元细胞体。6. 在营养不良小鼠中,神经冲动在纤维之间传递(“串扰”)。神经纤维之间冲动传递的部位靠近脊髓根的远端部分。7. 刺激背根诱发的突触电位和外周反射放电在营养不良小鼠中比对照小鼠具有更长的潜伏期且持续时间更长。8. 63 至 148 日龄的营养不良小鼠运动神经元特性无随年龄逐渐变化的趋势。9. 得出的结论是,在营养不良小鼠中检测到的运动神经元细胞体特性与正常小鼠的无法区分,并且前者运动神经元中唯一的异常存在于运动轴突中。10. 有人提出,营养不良小鼠脊髓运动神经元放电模式的完整性受到运动轴突中异常冲动传递的干扰,并且营养不良小鼠中的运动神经元是一个同质群体,而不是“正常”和“异常”神经元的混合体。

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