McQuarrie I G
J Comp Neurol. 1985 Jan 8;231(2):239-49. doi: 10.1002/cne.902310211.
The effect of a conditioning lesion on the time-course of axonal sprout formation after a subsequent testing lesion was evaluated in myelinated axons of the rat sciatic nerve. Transmission electron microscopy of longitudinal nerve sections was used to examine nodes of Ranvier located 200-500 micron proximal to the testing lesion. The conditioning lesion was a cut of the tibial nerve at the ankle; the testing lesion, made 2 weeks later, was a crush of the sciatic nerve at the hip. Sprouts were defined as unmyelinated evaginations of the nodal axolemma that (1) had reached the basement membrane of the Schwann cell, and (2) were located between the myelin sheath of the distal paranode and the basement membrane. Photomicrographs of the nodes at 9, 18, and 27 hours after the testing lesion were assigned to one of seven categories: normal, retracted, myelin degeneration, axonal degeneration, type A sprout formation (cytoskeleton absent), type B sprout formation (cytoskeleton present), and type B sprout degeneration. By 9 hours after the testing lesion, type B sprout formation was found in 9% of the nodes in control nerves (testing lesion alone) and 33% of those in conditioned nerves (P less than .01). A 33% incidence of type B sprout formation was not reached in control nerves until 27 hours after the testing lesion. Since the conditioning lesion was located 50 mm distal to the testing lesion and did not induce neuronal death, earlier sprout formation can be attributed to a neuronal response to the conditioning lesion rather than to a putative factor that arises from pre-degenerated fibers and acts on newly formed sprouts.
在大鼠坐骨神经的有髓轴突中,评估了预处理损伤对后续测试损伤后轴突发芽形成时间进程的影响。使用纵切神经切片的透射电子显微镜检查测试损伤近端200 - 500微米处的郎飞结。预处理损伤是在踝关节处切断胫神经;2周后进行的测试损伤是在髋关节处挤压坐骨神经。轴突芽被定义为结区轴膜的无髓鞘外翻,其(1)已到达施万细胞的基底膜,且(2)位于远端结旁区的髓鞘与基底膜之间。测试损伤后9小时、18小时和27小时的结区显微照片被分为七类之一:正常、回缩、髓鞘变性、轴突变性、A型芽形成(无细胞骨架)、B型芽形成(有细胞骨架)和B型芽变性。在测试损伤后9小时,对照神经(仅测试损伤)中9%的结区出现B型芽形成,而预处理神经中这一比例为33%(P < 0.01)。对照神经直到测试损伤后27小时才达到33%的B型芽形成发生率。由于预处理损伤位于测试损伤远端50毫米处且未诱导神经元死亡,更早的芽形成可归因于神经元对预处理损伤的反应,而非源于预先变性纤维并作用于新形成芽的假定因子。