Electrophysiological properties of spinal motoneurones of normal and dystrophic mice.
Electrophysiological properties of spinal motoneurones of normal and dystrophic mice.
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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。
DOI：
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发表时间：
1975
期刊：
影响因子：
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通讯作者：
Y. Miyata
中科院分区：
文献类型：
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作者：
P. Huizar;M. Kuno;Y. Miyata
1.用细胞内电极法观察了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没有显着差异：静息和动作电位，后超极化的幅度和持续时间，兴奋的电流，体细胞膜的兴奋阈值（IS-SD膜）和输入电阻。3.在正常和营养不良小鼠中，坐骨神经切片（轴突切断术）后13-16天观察到的运动神经元特性的变化相似。4.营养不良小鼠运动神经元轴突传导速度比正常小鼠慢10倍左右。坐骨神经的传导速度在营养不良小鼠中仅比正常动物慢约25%。估计的前根传导速度，以及观察到的背根传导速度在营养不良的小鼠至少是在正常小鼠的20倍慢。5.在营养不良的小鼠，脊髓运动神经元往往表现出多个放电响应单一，逆向刺激。多重放电的起始部位位于运动轴突而不是运动神经元胞体。6.在营养不良的小鼠中，神经冲动从纤维传递到纤维（“串扰”）。神经纤维之间的冲动传递部位在脊神经根远端附近。7.突触电位和外周反射放电引起的背根刺激表现出较长的潜伏期和营养不良小鼠比对照组小鼠延长。8.在63 ~ 148日龄范围内，营养不良小鼠的运动神经元特性无进行性变化的趋势。9.它的结论是，在营养不良的小鼠中检查的运动神经元细胞体的属性是无法区分的，从那些在正常小鼠和运动神经元的前残留物中的运动轴突的唯一异常。10.这表明，在营养不良的小鼠脊髓运动神经元的放电模式的完整性被干扰异常脉冲传输的运动轴突和营养不良的小鼠的运动神经元是一个同质的组，而不是“正常”和“异常”的神经元的混合物。
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.