Snyaptic and dendritic development and mental defect.

P R Huttenlocher
{"title":"Snyaptic and dendritic development and mental defect.","authors":"P R Huttenlocher","doi":"10.1016/b978-0-12-139050-1.50013-6","DOIUrl":null,"url":null,"abstract":"<p><p>The hypothesis that specific defects in synaptic and dendritic development of cerebral cortex may form the anatomical basis in some cases of mental defect has been examined by electron microscopy and by use of the Golgi-Cos method. Two types of abnormality have been identified to date. One is a specific lesion of presynaptic terminals, first reported by Gonatas and Goldensohn (14) in a child with mental retardation and myoclonic seizures. This lesion, consisting of massive proliferation of membranous structures in terminal axons, appears to be rare and may be the anatomical substrate of one or more genetically determined dementing illnesses in infancy. More commonly, cerebral cortex from the severely retarded shows defects in number, length, and spatial arrangement of dendrites and synapses, best demonstrated by the Golgi method. Such abnormalities have been found in six out of eleven brains from severely retarded individuals examined by us. The etiology of the retardation was unknown in the majority; two had other recognizable developmental malformations of brain. It is suggested that a number of different etiological factors, if active during the period of rapid synaptic and dendritic growth in cerebral cortex (i. e., from the last trimester of pregnancy to the end of the first postnatal year) may result in stunted development of these structures.</p>","PeriodicalId":76774,"journal":{"name":"UCLA forum in medical sciences","volume":" 18","pages":"123-40"},"PeriodicalIF":0.0000,"publicationDate":"1975-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"51","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"UCLA forum in medical sciences","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1016/b978-0-12-139050-1.50013-6","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 51

Abstract

The hypothesis that specific defects in synaptic and dendritic development of cerebral cortex may form the anatomical basis in some cases of mental defect has been examined by electron microscopy and by use of the Golgi-Cos method. Two types of abnormality have been identified to date. One is a specific lesion of presynaptic terminals, first reported by Gonatas and Goldensohn (14) in a child with mental retardation and myoclonic seizures. This lesion, consisting of massive proliferation of membranous structures in terminal axons, appears to be rare and may be the anatomical substrate of one or more genetically determined dementing illnesses in infancy. More commonly, cerebral cortex from the severely retarded shows defects in number, length, and spatial arrangement of dendrites and synapses, best demonstrated by the Golgi method. Such abnormalities have been found in six out of eleven brains from severely retarded individuals examined by us. The etiology of the retardation was unknown in the majority; two had other recognizable developmental malformations of brain. It is suggested that a number of different etiological factors, if active during the period of rapid synaptic and dendritic growth in cerebral cortex (i. e., from the last trimester of pregnancy to the end of the first postnatal year) may result in stunted development of these structures.

snytic和dendritic的发育和智力缺陷。
利用电子显微镜和高尔基-高斯方法,研究了大脑皮层突触和树突发育的特定缺陷可能构成某些精神缺陷病例的解剖学基础的假设。到目前为止,已经确定了两种类型的异常。一种是突触前终末的特异性病变,Gonatas和Goldensohn(14)首次报道了一种智力低下和肌阵挛性癫痫患儿的病变。这种病变由终端轴突的膜质结构的大量增生组成,似乎很罕见,可能是婴儿期一种或多种遗传决定的痴呆疾病的解剖学基础。更常见的是,严重智障者的大脑皮层在树突和突触的数量、长度和空间排列上都存在缺陷,高尔基方法最能证明这一点。在我们检查的11个严重弱智个体中,有6个大脑中发现了这种异常。大多数发育迟缓的病因不明;其中两人还有其他可识别的脑部发育畸形。这表明,如果在大脑皮层突触和树突快速生长期间(即从怀孕的最后三个月到出生后第一年末)活跃,许多不同的病因因素可能导致这些结构发育迟缓。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
自引率
0.00%
发文量
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:604180095
Book学术官方微信