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无髓鞘大鼠脊髓中损伤诱导的皮质脊髓纤维发芽增加。

Increased lesion-induced sprouting of corticospinal fibres in the myelin-free rat spinal cord.

作者信息

Vanek P, Thallmair M, Schwab M E, Kapfhammer J P

机构信息

Institut für Hirnforschung, Universität Zürich, Switzerland.

出版信息

Eur J Neurosci. 1998 Jan;10(1):45-56. doi: 10.1046/j.1460-9568.1998.00018.x.

DOI:10.1046/j.1460-9568.1998.00018.x
PMID:9753112
Abstract

Myelin contains potent inhibitors of neurite growth which have been implicated in the failure of long-distance regeneration of nerve fibres within the CNS. These myelin-associated neurite growth inhibitors may also be involved in the stabilization of neural connections by suppressing sprouting and fibre growth. After lesions of the CNS in neonatal animals, extensive rearrangements of the remaining fibre systems have been observed. In the rat, this plasticity of neuronal connections is severely restricted following the first few weeks of postnatal life, coincident with the progression of myelination of the nervous system. A well-studied example of postnatal plasticity is the sprouting of one corticospinal tract (CST) into the denervated half of the spinal cord after unilateral motor cortex or pyramidal lesions. In the hamster and rat, significant CST sprouting is restricted to the first 10 postnatal days. Here we show that very extensive sprouting of corticospinal fibres occurs after deafferentations as late as P21 if myelination is prevented by neonatal X-irradiation in the rat lumbar spinal cord. Sprouted fibres from the intact CST cross the midline and develop large terminal arbors in the denervated spinal cord, suggesting the establishment of synaptic connections. Our results suggest that myelin and its associated neurite growth inhibitors play an important role in the termination of neurite growth permissive periods during postnatal CNS development. Corticospinal sprouting subsequent to lesions early in life, i.e. in the absence of myelin-associated neurite growth inhibitors may explain the frequent occurrence of mirror movements in patients with hemiplegic cerebral palsy.

摘要

髓磷脂含有强大的神经突生长抑制剂,这些抑制剂被认为与中枢神经系统内神经纤维的长距离再生失败有关。这些髓磷脂相关的神经突生长抑制剂也可能通过抑制发芽和纤维生长参与神经连接的稳定。在新生动物的中枢神经系统受损后,已观察到剩余纤维系统的广泛重排。在大鼠中,神经元连接的这种可塑性在出生后的头几周后受到严重限制,这与神经系统髓鞘形成的进展相一致。一个经过充分研究的出生后可塑性的例子是,在单侧运动皮层或锥体损伤后,一条皮质脊髓束(CST)向脊髓去神经支配的一半发芽。在仓鼠和大鼠中,显著的CST发芽仅限于出生后的前10天。在这里,我们表明,如果通过新生大鼠腰椎脊髓的X射线照射阻止髓鞘形成,那么在P21时去传入后,皮质脊髓纤维会发生非常广泛的发芽。来自完整CST的发芽纤维穿过中线,并在去神经支配的脊髓中形成大的终末分支,这表明建立了突触连接。我们的结果表明,髓磷脂及其相关的神经突生长抑制剂在出生后中枢神经系统发育过程中神经突生长许可期的终止中起重要作用。生命早期损伤后的皮质脊髓发芽,即在没有髓磷脂相关神经突生长抑制剂的情况下,可能解释了偏瘫性脑瘫患者中镜像运动的频繁发生。

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