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Glial membrane specializations in extraparanodal regions.

作者信息

Rosenbluth J

出版信息

J Neurocytol. 1978 Dec;7(6):709-19. doi: 10.1007/BF01205146.

DOI:10.1007/BF01205146
PMID:310449
Abstract

Previous freeze-fracture studies of central myelinated nerve fibres have demonstrated a distinctive junction in the paranodal region formed between the terminal loops of the glial cell and the axolemma. This unique junction is characterized by the presence of diagonally oriented rows of particles in the P face and to a lesser extent in the E face of the glial cell and an equivalent pattern in the axolemma. In both, the rows are spaced at 250--300 A intervals. Although this junction was originally thought to be peculiar to the paranodal region, examples of the same pattern have now been seen in extraparanodal regions in the central nervous system where they appear as circumscribed patches of membrane exhibiting a pattern identical to that in the paranodal glial loops. All examples found were in the immediate vicinity of myelinated nerve fibres and in one case the membrane containing the specialized patch was identified as a lamella of a myelin sheath. These observations constitute evidence that this distinctive membrane specialization is not limited to the paranodal axoglial junction but can also be found in glial membrane specialization is not limited to the paranodal axoglial junction but can also be found in glial membranes not in immediate contact with the specialized membrane of the paranodal axolemma.

摘要

相似文献

1
Glial membrane specializations in extraparanodal regions.
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引用本文的文献

1
Histopathological heterogeneity of neuropathy in insulin-dependent and non-insulin-dependent diabetes, and demonstration of axo-glial dysjunction in human diabetic neuropathy.胰岛素依赖型和非胰岛素依赖型糖尿病中神经病变的组织病理学异质性,以及人类糖尿病性神经病变中轴突-神经胶质分离的证明。
J Clin Invest. 1988 Feb;81(2):349-64. doi: 10.1172/JCI113327.
2
Axo-glial dysjunction. A novel structural lesion that accounts for poorly reversible slowing of nerve conduction in the spontaneously diabetic bio-breeding rat.轴突-神经胶质分离。一种新的结构损伤,可解释自发性糖尿病生物繁殖大鼠神经传导不可逆性减慢的原因。
J Clin Invest. 1986 Feb;77(2):474-84. doi: 10.1172/JCI112326.