Davis F A, Jacobson S
J Neurol Neurosurg Psychiatry. 1971 Oct;34(5):551-61. doi: 10.1136/jnnp.34.5.551.
Electrophysiological studies were performed on frog and guinea-pig peripheral nerves to determine the effect of temperature on conduction at the site of pressure and demyelinating lesions. An increased susceptibility to thermally-induced conduction blockade has been demonstrated. In pressure-injured frog and guinea-pig nerves, conduction blocks occur at temperatures approximately 6°C lower than in normal nerves. A similar phenomenon occurs in guinea-pig demyelinated nerve (experimental allergic neuritis) and in some cases at temperatures around 15°C lower than in controls. It is suggested that these effects are the result of a critical lowering by temperature of an already markedly depressed conduction safety factor. In support of this, it has been shown that calcium ion depletion, which would be expected to increase the conduction safety factor by lowering the threshold for excitation, counteracts the increased thermal sensitivity of frog pressure-injured nerve. These findings are discussed in relation to well-known temperature effects in multiple sclerosis. They add support to an earlier proposed hypothesis that the changes in signs and symptoms with a change of body temperature in multiple sclerosis may be caused by an effect of temperature on axonal conduction.
对青蛙和豚鼠的外周神经进行了电生理研究,以确定温度对压力性和脱髓鞘性病变部位传导的影响。研究表明,热诱导传导阻滞的易感性增加。在压力损伤的青蛙和豚鼠神经中,传导阻滞发生的温度比正常神经低约6°C。类似的现象也发生在豚鼠脱髓鞘神经(实验性变应性神经炎)中,在某些情况下,发生传导阻滞的温度比对照组低约15°C。有人认为,这些效应是由于温度使已经明显降低的传导安全系数临界降低所致。支持这一观点的是,已经表明,钙离子耗竭,预计会通过降低兴奋阈值来增加传导安全系数,可抵消青蛙压力损伤神经增加的热敏感性。结合多发性硬化症中众所周知的温度效应讨论了这些发现。它们为早期提出的假说提供了支持,即多发性硬化症中体征和症状随体温变化可能是温度对轴突传导产生影响所致。