Saito A, Kasuya Y, Goto K
J Pharmacol Exp Ther. 1981 May;217(2):516-23.
Local application of colchicine to the hypogastric plexus produced degenerative changes in about 40% of adrenergic nerve endings and a decrease in the neuromuscular transmission in the rat vas deferens. Unlike after denervation, both decreases in the number of normal nerve terminals and neuromuscular transmission induced by colchicine were incomplete and reversible. Although the time course of these changes was apparently related to that of the development of supersensitivity after colchicine treatment, the degeneration of adrenergic nerves does not seem to be an essential factor for the manifestation of colchicine-induced supersensitivity which is quantitatively and qualitatively identical to that induced by denervation. It is suggested that some neurotrophic factor(s) may contribute to the control of responsiveness of the smooth muscle and that the denervation-like supersensitivity is induced by colchicine through an interference of axonal transport in adrenergic nerves.
将秋水仙碱局部应用于大鼠腹下神经丛,约40%的肾上腺素能神经末梢出现退行性变化,且大鼠输精管的神经肌肉传递功能降低。与去神经支配后不同,秋水仙碱引起的正常神经末梢数量减少和神经肌肉传递功能降低均不完全且可逆。尽管这些变化的时间进程显然与秋水仙碱治疗后超敏反应的发展过程相关,但肾上腺素能神经的退化似乎并非秋水仙碱诱导超敏反应表现的必要因素,后者在数量和质量上与去神经支配诱导的超敏反应相同。提示某些神经营养因子可能参与平滑肌反应性的调控,秋水仙碱通过干扰肾上腺素能神经的轴突运输诱导出类似去神经支配的超敏反应。