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蛙在沃勒变性过程中的血-神经屏障:轴突对于维持屏障功能是否必要?

Blood-nerve barrier in the frog during wallerian degeneration: are axons necessary for maintenance of barrier function?

作者信息

Latker C H, Wadhwani K C, Balbo A, Rapoport S I

机构信息

Laboratory of Neurosciences, National Institute on Aging, National Institutes of Health, Bethesda, Maryland 20892.

出版信息

J Comp Neurol. 1991 Jun 22;308(4):650-64. doi: 10.1002/cne.903080410.

Abstract

Blood-nerve barrier tissues (endoneurial blood vessels and perineurium) of the frog's sciatic nerve were studied during chronic Wallerian degeneration to determine whether barrier function depends on the presence of intact axons. Sciatic nerves of adult frogs were transected in the abdominal cavity; the ends were tied to prevent regeneration and the distal nerve stumps were examined. Vascular permeabilities to horseradish peroxidase and to [14C]sucrose increased to day 14, returned toward normal levels by 6 weeks, and continued at near normal levels to 9 months. Perineurial permeabilities to the tracers increased by day 10 and remained elevated at 9 months. Proliferation of perineurial, endothelial, and mast cells occurred between 3 days and 6 weeks, resulting in an increased vascular space (measured with [3H]dextran) and number of vascular profiles. The perineurium increased in thickness and the mast cells increased in number. This study indicates that during Wallerian degeneration of the frog's sciatic nerve there is 1) a transitory increase in vascular permeability distal to the lesion, that is related to changes within the endoneurium; 2) an irreversible increase in permeability of the perineurium, which begins later than that seen in the endoneurial blood vessels; and 3) proliferation of non-neuronal components in the absence of regenerating neuronal elements. The results indicate that maintenance of vascular integrity does not require the presence of axons in the frog's peripheral nerve, whereas perineurial integrity and barrier function are affected irreversibly by Wallerian degeneration.

摘要

在慢性沃勒变性过程中,对青蛙坐骨神经的血神经屏障组织(神经内膜血管和神经束膜)进行了研究,以确定屏障功能是否依赖于完整轴突的存在。成年青蛙的坐骨神经在腹腔内被切断;将两端扎起来以防止再生,并检查远端神经残端。辣根过氧化物酶和[14C]蔗糖的血管通透性在第14天增加,到6周时恢复到正常水平,并在9个月内维持在接近正常的水平。示踪剂的神经束膜通透性在第10天增加,并在9个月时保持升高。神经束膜、内皮细胞和肥大细胞在3天至6周之间发生增殖,导致血管间隙(用[3H]葡聚糖测量)和血管轮廓数量增加。神经束膜厚度增加,肥大细胞数量增加。这项研究表明,在青蛙坐骨神经的沃勒变性过程中,1)病变远端的血管通透性有短暂增加,这与神经内膜内的变化有关;2)神经束膜通透性有不可逆增加,其开始时间晚于神经内膜血管;3)在没有再生神经元成分的情况下,非神经元成分发生增殖。结果表明,青蛙周围神经中血管完整性的维持不需要轴突的存在,而沃勒变性会不可逆地影响神经束膜的完整性和屏障功能。

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