Dendritic spine dysgenesis in autism related disorders

被引：138

作者：

Phillips, Mary ^{[1
]}

Pozzo-Miller, Lucas ^{[1
]}

机构：

[1] Univ Alabama Birmingham, Dept Neurobiol, Civitan Int Res Ctr, Birmingham, AL 35294 USA

来源：

NEUROSCIENCE LETTERS | 2015年 / 601卷

关键词：

mTOR; mGluR; TrkB; Fragile X; Rett syndrome; MeCP2; Intellectual disability; LONG-TERM POTENTIATION; FRAGILE-X-SYNDROME; MENTAL-RETARDATION PROTEIN; NEUROTROPHIC FACTOR EXPRESSION; DEPENDENT SYNAPTIC PLASTICITY; MOUSE MODEL; TUBEROUS SCLEROSIS; RETT-SYNDROME; DOWN-SYNDROME; ANGELMAN-SYNDROME;

D O I：

10.1016/j.neulet.2015.01.011

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

The activity-dependent structural and functional plasticity of dendritic spines has led to the long-standing belief that these neuronal compartments are the subcellular sites of learning and memory. Of relevance to human health, central neurons in several neuropsychiatric illnesses, including autism related disorders, have atypical numbers and morphologies of dendritic spines. These so-called dendritic spine dysgeneses found in individuals with autism related disorders are consistently replicated in experimental mouse models. Dendritic spine dysgenesis reflects the underlying synaptopathology that drives clinically relevant behavioral deficits in experimental mouse models, providing a platform for testing new therapeutic approaches. By examining molecular signaling pathways, synaptic deficits, and spine dysgenesis in experimental mouse models of autism related disorders we find strong evidence for mTOR to be a critical point of convergence and promising therapeutic target. (C) 2015 Elsevier Ireland Ltd. All rights reserved.

引用

页码：30 / 40

页数：11

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