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新生大鼠酸性磷酸酶(FRAP)传入终末场和背角细胞生长的可塑性。

Plasticity of acid phosphatase (FRAP) afferent terminal fields and of dorsal horn cell growth in the neonatal rat.

作者信息

Fitzgerald M, Vrbová G

机构信息

Department of Anatomy, University College London, United Kingdom.

出版信息

J Comp Neurol. 1985 Oct 22;240(4):414-22. doi: 10.1002/cne.902400409.

Abstract

Peripheral nerve section results in depletion of fluoride-resistant acid phosphatase (FRAP) from the nerve terminals in the dorsal horn of the spinal cord (Schoenen et al., '68) and this has been used in the past to map the termination field of individual nerves (Rustioni et al., '71; Devor and Claman, '80). In the present study we show that a similar central depletion occurs following sciatic nerve section or crush in neonatal rats. Unlike adults, however, the area of depletion is rapidly filled by sprouting of FRAP-containing afferent terminals from nearby intact peripheral nerves. The sprouting is extensive but never completely fills the depleted area. After nerve crush there is some recovery of FRAP from the sciatic nerve terminals themselves as well as from nearby nerve terminals. The source of recovered FRAP is demonstrated by resectioning or recrushing the nerves. The sprouting occurred when the sciatic was injured on day 1 but failed to take place when the injury was applied on or after day 10. Sciatic nerve section on day 1 also produces marked growth retardation of the ipsilateral dorsal horn gray matter that becomes more apparent as the rat matures. Nerve crush produces a less marked shrinkage that is slower in onset. If the nerve is crushed repeatedly, however, so that regeneration is prevented, the shrinkage is analogous to that following nerve section. No shrinkage occurs if the nerve is cut or crushed on day 10. The results show that separation of the spinal cord from its peripheral input at a critical stage in development results in disruption of the somatotopic organization of the C fibre afferent input to the dorsal horn and in slowing of growth of the dorsal horn gray matter.

摘要

外周神经切断会导致脊髓背角神经终末的耐氟酸性磷酸酶(FRAP)减少(舍嫩等人,1968年),过去曾利用这一点来描绘各条神经的终末区域(鲁斯蒂奥尼等人,1971年;德沃尔和克拉曼,1980年)。在本研究中,我们发现新生大鼠坐骨神经切断或挤压后,脊髓背角也会出现类似的神经终末FRAP减少。然而,与成年动物不同的是,减少区域会迅速被来自附近完整外周神经的含FRAP传入终末的芽生所填充。芽生范围广泛,但从未完全填满减少区域。神经挤压后,坐骨神经终末本身以及附近神经终末的FRAP会有一定程度的恢复。通过再次切断或挤压神经证明了恢复的FRAP的来源。芽生在出生第1天坐骨神经受伤时出现,但在第10天或之后受伤时则不会发生。出生第1天切断坐骨神经还会导致同侧脊髓背角灰质明显生长迟缓,且随着大鼠成熟愈发明显。神经挤压造成的萎缩不太明显,且开始时间较晚。然而,如果反复挤压神经以阻止其再生,萎缩情况则类似于神经切断后的情况。在出生第10天切断或挤压神经则不会出现萎缩。结果表明,在发育的关键阶段切断脊髓与外周输入的联系,会导致C纤维传入至背角的躯体定位组织紊乱,并使背角灰质生长减缓。

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