Slack J R, Hopkins W G, Williams M N
Nature. 1979 Nov 29;282(5738):506-7. doi: 10.1038/282506a0.
When disease or injury causes partial loss of innervation from a muscle, the remaining axons sprout and form new connections to the denervated muscle fibres. Sprouting can occur in two ways: from axon terminals (terminal sprouting) or from the intramuscular axons themselves, probably from the nodes of Ranvier (collateral sprouting). Terminal sprouting has been induced experimentally using various methods, including partial denervation, nerve conduction block and nerve transmission block. A common factor in the induction of terminal sprouting seems to be changes in the surface membrane of muscle fibres; these changes and terminal sprouting are prevented by direct stimulation of the muscle. Collateral sprouting has been induced only by partial denervation and is not prevented by direct stimulation. This has been taken as evidence for an earlier suggestion that products of nerve or axon degeneration may be a direct stimulus for collateral sprouting. We report here that axon degeneration products alone are probably not the stimulus for collateral sprouting.
当疾病或损伤导致肌肉的神经支配部分丧失时,剩余的轴突会发芽并与失神经支配的肌纤维形成新的连接。发芽可以通过两种方式发生:从轴突末端(终末发芽)或从肌内轴突本身,可能从郎飞结(侧支发芽)。终末发芽已通过多种方法在实验中诱导产生,包括部分去神经支配、神经传导阻滞和神经传递阻滞。诱导终末发芽的一个共同因素似乎是肌纤维表面膜的变化;这些变化和终末发芽可通过直接刺激肌肉来预防。侧支发芽仅通过部分去神经支配诱导产生,并且不能通过直接刺激来预防。这被视为早期观点的证据,即神经或轴突退化的产物可能是侧支发芽的直接刺激因素。我们在此报告,仅轴突退化产物可能不是侧支发芽的刺激因素。