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突触发育不全。

Synaptic dysgenesis.

作者信息

Becker L E

机构信息

Department of Pathology, University of Toronto, Ontario.

出版信息

Can J Neurol Sci. 1991 May;18(2):170-80. doi: 10.1017/s0317167100031644.

DOI:10.1017/s0317167100031644
PMID:1829978
Abstract

Synapse formation is a complex, incompletely understood process that has received only limited investigation in man despite the importance of synaptic dysfunction in common disorders such as epilepsy and mental retardation. This review explores synaptic differentiation, focussing on the morphologic maturation of synapses. Since differentiation depends on many antecedent developmental events, synaptogenesis can be affected by several factors: errors in neuronal proliferation, migration, and differentiation. The challenge to the neurobiologist is to detect and evaluate the minor alterations in neuronal differentiation that could account for the structural basis of the clinical manifestations. Trisomy 21 is an example of a condition in which the cytoarchitecture of the cerebral cortex is not obviously altered, yet mental retardation is consistently present; research neurobiologic techniques are making possible documentation of its structural basis. Epilepsy is another example in which examination of surgically removed cerebral cortex reveals subtle cortical dysplasias helpful in understanding the basis for the abnormal electrical discharge. Further exploration of synaptogenesis, particularly the influence of gene products and epigenetic factors on synapse maturation, will increase our understanding of the pathogenesis of conditions in which "morphology" seems normal but function is abnormal.

摘要

突触形成是一个复杂且尚未完全被理解的过程,尽管突触功能障碍在癫痫和智力迟钝等常见疾病中很重要,但在人类中对此的研究仍然有限。这篇综述探讨突触分化,重点关注突触的形态成熟。由于分化依赖于许多先前的发育事件,突触发生会受到多种因素的影响:神经元增殖、迁移和分化过程中的错误。神经生物学家面临的挑战是检测和评估神经元分化中的微小变化,这些变化可能是临床表现的结构基础。21三体综合征就是一个例子,在这种情况下,大脑皮质的细胞结构没有明显改变,但智力迟钝却一直存在;神经生物学研究技术正在使记录其结构基础成为可能。癫痫是另一个例子,对手术切除的大脑皮质进行检查发现了细微的皮质发育异常,这有助于理解异常放电的基础。对突触发生的进一步探索,特别是基因产物和表观遗传因素对突触成熟的影响,将增进我们对那些“形态”看似正常但功能异常的疾病发病机制的理解。

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Consequences of trisomy 16 for mouse brain development: corticogenesis in a model of Down syndrome.16号染色体三体对小鼠大脑发育的影响:唐氏综合征模型中的皮质发生
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