EXTENSION OF THE CRITICAL PERIOD FOR DEVELOPMENTAL PLASTICITY OF THE CORTICOSPINAL PATHWAY
EXTENSION OF THE CRITICAL PERIOD FOR DEVELOPMENTAL PLASTICITY OF THE CORTICOSPINAL PATHWAY
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DOI：
10.1002/cne.902820304
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发表时间：
1989-04-15
影响因子：
2.5
通讯作者：
ONEILL, A
中科院分区：
文献类型：
--
作者：
BREGMAN, BS;KUNKELBAGDEN, E;ONEILL, A
皮质脊髓束（CST）的比率经历了长时间的出生后发育。出生时推定的 CST 通路损伤后，损伤部位周围正在发育的皮质脊髓轴突通过邻近未损伤的中枢神经系统组织异常重新路由。这种发育可塑性在 5-6 天龄时受到严重限制，因此轴突不再能够在损伤部位周围生长。本研究的目的是确定通过用移植的胎儿脊髓组织填充病变来改变损伤部位的环境是否可以延长皮质脊髓通路发育可塑性的关键期。脊髓在皮质脊髓 (CS) 通路发育的三个阶段受到损伤（过度半切）：1）在 CS 轴突到达之前，2）在轴突伸长穿过脊髓后突触发生之前，以及 3）在轴突伸长和突触发生完成后。 1 至 9 个月后，使用辣根过氧化物酶顺行神经元示踪来评估损伤部位有或没有胎儿移植的皮质脊髓通路的生长，并将标记模式与成年未损伤对照动物中观察到的标记模式进行比较。我们的结果表明 CST 的存在。在整个产后检查期间，移植引起了 cST 轴突的生长。突触发生前受损的 CST 轴突比突触发生完成后受损的轴突表现出更强劲的生长。这些结果表明，环境因素和神经元因素相互作用，调节未成熟 CS 神经元对损伤的反应。
The corticospinal tract (CST) of the rate undergoes a prolonged period of postnatal development. Lesions of the presumptive CST pathway at birth are followed by the aberrant rerouting of the developing corticospinal axons around the lesion site through adjacent undamaged CNS tissue. This developmental plasticity becomes severely restricted by 5-6 days of age, so the axons are no longer capable of growth around the site of injury. The aim of the current study to determine whether altering the environment at the site of injury by filling the lesion with transplanted fetal spinal cord tissue could prolong the critical period for the developmental plasticity of the corticospinal pathway. The spinal cord was damaged (overhemisection) at three stages in the developmment of the corticospinal (CS) pathway: 1) prior to the arrival of CS axons, 2) after the axons elongated through the cord put prior to synaptogenesis, and 3) after both axonal elongation and synaptogenesis were completed. One to 9 months later, anterograde neuronal tracing with horseradish peroxidase was used to assess the growth of the corticospinal pathway with or without a fetal transplant at the site of injury, and the pattern of labeling was compared with that observed in adult nonlesioned control animals. Our results indicate that the presence of the CST. Transplants elicited growth of cST axons throughout the postnatal period examined. CST axons damaged prior to synaptogenesis exhibited more robust growth than those lesioned after synaptogenesis had been completed. These results suggest that both environmental and neuronal factors interact to regulate the response of immature CS neurons to injury.