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小鼠指小体的退变

Degeneration of mouse digital corpuscles.

作者信息

Idé C

出版信息

Am J Anat. 1982 Jan;163(1):59-72. doi: 10.1002/aja.1001630105.

Abstract

The sequential changes of the morphology and the histochemically demonstrated, nonspecific cholinesterase (ChE) activity of the denervated digital corpuscle (Meissner corpuscle) of the mouse were observed by light and electron microscopy for 6 months after transection of the sciatic nerve. A fragment of the sciatic nerve, approximately 1 cm long, was removed from the distal stump to prevent reinnervation. Within one day following nerve division, the axon terminals began to manifest degenerative changes: the axoplasm became electron-opaque and some mitochondria became disorganized. The lamellar cell processes (lamellar) also exhibited atrophic changes: they became thinner and more electron opaque. The lamellar cell body became smaller due to a decreased amount of cytoplasm and contained few organelles except for some free ribosomes. These changes advance with time. Around 4-6 months after denervation, the corpuscle was small, consisting of a few thin, shrunken, atrophic lamellar cells. The ChE activity persisted and could be demonstrated in the interlamellar spaces, but its intensity decreased with time so that the corpuscle was hardly identifiable by light microscope histochemistry around 4-6 months after denervation. During this time, the precipitates of the reaction product were scattered as small particles throughout the interlamellar spaces. The enzyme activity in the cisternae of the rough endoplasmic reticulum and the nuclear envelope of the lamellar cell body was no longer demonstrable 5 days or less after denervation. These findings indicate that the lamellar cell is dependent on the axon terminal to maintain its normal morphology and the function of ChE synthesis.

摘要

在坐骨神经横断后,通过光镜和电镜观察小鼠失神经支配的指小体(迈斯纳小体)形态和组织化学显示的非特异性胆碱酯酶(ChE)活性的连续变化,为期6个月。从远侧断端切除约1cm长的一段坐骨神经,以防止再支配。神经切断后1天内,轴突终末开始出现退行性变化:轴浆变得电子密度增高,一些线粒体变得紊乱。板层细胞突起(板层)也表现出萎缩性变化:它们变得更细且电子密度更高。板层细胞体由于细胞质减少而变小,除了一些游离核糖体外几乎没有细胞器。这些变化随时间进展。失神经支配后约4 - 6个月,小体变小,由少数薄的、皱缩的、萎缩的板层细胞组成。ChE活性持续存在,可在板层间隙中显示,但其强度随时间降低,以至于在失神经支配后约4 - 6个月,通过光镜组织化学几乎无法识别小体。在此期间,反应产物沉淀以小颗粒形式散布在整个板层间隙中。失神经支配5天或更短时间后,板层细胞体粗面内质网池和核膜中的酶活性不再能显示。这些发现表明板层细胞依赖轴突终末来维持其正常形态和ChE合成功能。

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