ULTRASTRUCTURAL STUDIES OF DYING-BACK PROCESS .2. SEQUESTRATION AND REMOVAL BY SCHWANN-CELLS AND OLIGODENDROCYTES OF ORGANELLES FROM NORMAL AND DISEASED AXONS
ULTRASTRUCTURAL STUDIES OF DYING-BACK PROCESS .2. SEQUESTRATION AND REMOVAL BY SCHWANN-CELLS AND OLIGODENDROCYTES OF ORGANELLES FROM NORMAL AND DISEASED AXONS
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DOI：
10.1007/bf01097197
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发表时间：
1974-01-01
期刊：
影响因子：
--
通讯作者：
THOMAS, PK
中科院分区：
文献类型：
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作者：
SPENCER, PS;THOMAS, PK
一种机制是假设和描述的隔离和吞噬不寻常的和异常的轴浆细胞器的雪旺氏细胞和少突胶质细胞。参与这一过程的轴突细胞器是清晰而致密的核心囊泡，膜结合的致密膜体，使人联想到次级溶酶体，扩大的线粒体，糖原样颗粒和充满糖原的线粒体残余物。隔离这些细胞器的过程开始于形成一个脊的成鞘细胞轴索细胞质相邻的轴膜的内部涂层区域。轴索细胞器附近的轴索表面细胞质嵴变大，形成薄片状突起。内陷的轴突细胞质片包围异常的轴突细胞器，并将它们与轴突的其余部分隔离。细胞质片向内折叠，并隔离轴浆细胞器组，形成交叉的剖面图。电子透明区对应于被隔离的轴质，电子致密区对应于成鞘细胞的细胞质。在叉指状网络中分离轴浆和成鞘细胞胞质的膜破裂，使得异常的轴浆细胞器被成鞘细胞胞质吞噬。该过程在正常神经系统的副阳极发生有限程度，但在有早期轴突疾病的病理情况下更发达。这个过程最大限度地发展的情况下，有向心轴突变性，如发生在dying-back中毒性疾病和近端残端的截肢神经。
A mechanism is postulated and described for the sequestration and phagocytosis of unusual and abnormal axoplasmic organelles by Schwann and oligodendroglial cells. Axonal organelles involved in this process are clear and dense-core vesicles, membrane-bounded dense membranous bodies reminiscent of secondary lysosomes, enlarged mitochondria, glycogen-like granules and glycogen-filled mitochondrial remnants. The process of sequestration of these organelles begins with the formation of a ridge of ensheathing cell adaxonal cytoplasm adjacent to an internally coated region of axolemma. The ridge of adaxonal cytoplasm enlarges to form a thin sheet which indents the axon surface adjacent to the abnormal axonal organelles. The invaginating adaxonal cytoplasmic sheet surrounds the abnormal axonal organelles and segregates them from the remainder of the axon. The cytoplasmic sheet infolds on itself and sequesters groups of axoplasmic organelles to form an interdigitated profile when viewed in cross-section. Electron lucent areas correspond to sequestered axoplasm and electron dense areas to ensheathing cell cytoplasm. The membranes separating axoplasm and ensheathing cell cytoplasm in the interdigitated networks break down allowing the abnormal axoplasmic organelles to be phagocytosed by the ensheathing cell cytoplasm. The process occurs to a limited degree in the normal nervous system at paranodes but is much more developed in pathologic situations where there is early axonal disease. The process is maximally developed in situations where there is centripetal axonal degeneration such as occurs in dying-back toxic disease and in the proximal stump of an amputated nerve.