Stelzner D J, Strauss J A
J Comp Neurol. 1986 Mar 1;245(1):83-106. doi: 10.1002/cne.902450107.
The present study was designed to assess whether axon collateral formation and loss or retrograde cell death contribute to selective reinnervation during optic nerve regeneration in the frog, Rana pipiens. The right optic nerve was crushed in 18 frogs, and samples were taken near the optic disc (retinal segment) and near the optic chiasm (brain segment). These samples were studied quantitatively with the electron microscope at various postoperative survival times (1, 2, 3, 4, 6, 12 weeks, 6 months, 1 year; N = 2). The number and size of axons in each segment were estimated from a series of electron micrographs taken at intervals across the transverse extent of each nerve and compared with normal nerves (N = 4). Results show that there are 5.3 +/- 1.8 X 10(5) (S.D.) unmyelinated and 2.3 +/- .5 X 10(4) myelinated axons in the normal nerve. One week post-crush (p.c.) there is a 27% decrease in the number of axons in the retinal segment (4.1 +/- 1.4 X 10(5)), indicating early retrograde axonal loss. As expected, there is a greater loss of axons at this time in the brain segment (3.0 +/- 1.3 X 10(5)). Between 2 and 6 weeks p.c. the number of axons increases in the retinal segment to over twice the normal number of axons increases in the retinal segment to over twice the normal number (12.3 +/- 3.8 X 10(5)) and to over four times this number in the brain segment (20.0 +/- 3.0 X 10(5)), showing collateral axon formation results from this injury. A large loss in the number of axons occurs in both nerve segments between 6 and 12 weeks p.c. (4.3 +/- 1.5 X 10(5)) and an additional loss at 20 weeks p.c. (2.2 +/- .98 X 10(5)). Subsequently, the number remains constant, approximately 40% of normal. Visual recovery was seen in the two frogs tested one year after optic nerve crush that were used for optic axon counts. Autoradiography in these same animals showed the optic nerve projections normally seen after regeneration. Besides axonal loss, our results also indicate that the size of both myelinated and unmyelinated axons is significantly above normal at chronic postoperative periods. This increase in axonal size is interpreted to be related to the increased territory each remaining optic axon must fill to restore the optic projections.(ABSTRACT TRUNCATED AT 400 WORDS)
本研究旨在评估轴突侧支形成与丧失或逆行性细胞死亡是否有助于牛蛙视神经再生过程中的选择性再支配。18只牛蛙的右侧视神经被挤压，在视盘附近（视网膜段）和视交叉附近（脑段）取样。在术后不同存活时间（1、2、3、4、6、12周、6个月、1年；N = 2）用电子显微镜对这些样本进行定量研究。从横跨每条神经横向范围间隔拍摄的一系列电子显微照片中估计每个段轴突的数量和大小，并与正常神经（N = 4）进行比较。结果显示正常神经中有5.3±1.8×10⁵（标准差）条无髓鞘轴突和2.3±0.5×10⁴条有髓鞘轴突。挤压后1周，视网膜段轴突数量减少27%（4.1±1.4×10⁵），表明早期逆行性轴突丧失。正如预期，此时脑段轴突丧失更多（3.0±1.3×10⁵）。挤压后2至6周，视网膜段轴突数量增加到正常数量的两倍多（12.3±3.8×10⁵），脑段增加到正常数量的四倍多（20.0±3.0×10⁵），表明这种损伤导致了侧支轴突形成。挤压后6至12周，两个神经段的轴突数量大幅减少（4.3±1.5×10⁵），挤压后20周进一步减少（2.2±0.98×10⁵）。随后，数量保持恒定，约为正常数量的40%。在用于视神经轴突计数的视神经挤压一年后测试的两只牛蛙中观察到了视觉恢复。这些相同动物的放射自显影显示了再生后正常可见的视神经投射。除了轴突丧失，我们的结果还表明，在术后慢性期，有髓鞘和无髓鞘轴突的大小均显著高于正常。轴突大小的这种增加被解释为与每条剩余视神经轴突为恢复视觉投射必须填充的增加区域有关。（摘要截断于400字）
