Cell death of motoneurons in the chick embryo spinal cord. III. The differentiation of motoneurons prior to their induced degeneration following limb‐bud removal
Cell death of motoneurons in the chick embryo spinal cord. III. The differentiation of motoneurons prior to their induced degeneration following limb‐bud removal
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鸡胚脊髓中运动神经元的细胞死亡 III. 肢芽去除后运动神经元的分化。
DOI：
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发表时间：
1978
期刊：
影响因子：
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通讯作者：
J. Maderdrut
中科院分区：
文献类型：
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作者：
R. Oppenheim;I. Chu‐Wang;J. Maderdrut
研究了早期肢芽消融后运动神经元在鸡胚4天内的分化情况。在去除这些细胞的正常靶标后，发现23-29节段（腰椎）侧运动柱（LMC）中约90%的神经元消失。通过对退化细胞的计数表明，几乎所有的细胞损失都可以通过细胞死亡来解释，而不是增殖受损或从LMC迁移的增强。外周剥夺组和对照组之间细胞死亡的定量比较表明，肢芽切除不仅使该系统中已知的50%自然细胞死亡增加，而且大大加快了整个过程。到第30期（6.5 - 7天），75%的最终细胞损失发生在被剥夺的一侧，而只有40%的最终细胞损失发生在对照组一侧。然而，在这两种情况下，细胞死亡都局限于肢体神经支配期。外周被剥夺的腹根的轴突计数显示，所有被剥夺的神经元最初都向脊髓外发送了一个轴突。然而，其中大多数在到达肢体附着部位之前就被神经瘤缠住了。虽然在神经瘤中未发现突触，但轴突显示能够将HRP运输回脊髓。在它们开始退化之前，被剥夺的LMC运动神经元发育出树突状突起，这些突起能够与前侧白质中的轴突形成突触。在早期阶段，在脊髓被剥夺和控制侧的前侧白质中观察到频繁的轴索胶质“突触”。由于到第36期（第10天），这些几乎都消失了，这表明脊髓这一区域的突触形成最初可能受到很少的限制。在晚期（即第8天之后），我们注意到脊髓两侧侧白质中经常出现轴突变性的迹象，提示由早期运动神经元细胞死亡引发的逆行跨神经元变性。电镜检查在退变前不同阶段的LMC细胞未能发现它们与脊髓非剥夺侧的对照细胞之间有任何明显差异。
The differentiation of motoneurons following early limb‐bud ablation was studied in chick embryos from four days to hatching. Following the removal of the normal targets of these cells about 90% of the neurons in the lateral motor column (LMC) of segments 23–29 (lumbar) were found to disappear. By counting degenerating cells it was shown that virtually all of the cell loss could be accounted for by cell death, rather than impaired proliferation or enhanced migration away from the LMC. Quantitative comparisons of cell death between the peripherally deprived and the control, non‐deprived side demonstrated that limb‐bud removal not only enhanced the 50% natural cell death known to occur in this system, but also greatly accelerated the whole process. By stage 30 (6.5‐7 days) 75% of the final cell loss had occurred on the deprived side, whereas only 40% of the final cell loss had occurred on the control side. In both cases, however, cell death was confined to the period of limb innervation. Axon counts of the peripherally deprived ventral root showed that all the deprived neurons initially had sent an axon out of the spinal cord. Most of these, however, became caught in a neuroma before reaching the site of limb attachment. Though no synapses were found in the neuroma the axons were shown to be able to transport HRP back to the spinal cord. Before they began to degenerate, the deprived LMC motoneurons developed dendritic processes and these were able to form synapses with axons in the prospective lateral white matter. In early stages, frequent axo‐glial “synapses” were observed in the prospective lateral white matter of both deprived and control sides of the spinal cord. Since by stage 36 (day 10) these had virtually all disappeared, it was suggested that synapse formation in this region of the spinal cord may initially be under few constraints. In late stages (i.e., after day 8) it was noted that there were frequently signs of axonal degeneration in the lateral white matter on both sides of the spinal cord, suggesting a retrograde transneuronal degeneration initiated by the earlier cell death of motoneurons. Electron microscopic examination of the deprived LMC cells at different stages prior to degeneration failed to uncover any obvious differences between them and control cells on the non‐deprived side of the spinal cord.