Hippocampal pyramidal cells in adult Fmr1 knockout mice exhibit an immature-appearing profile of dendritic spines
Hippocampal pyramidal cells in adult Fmr1 knockout mice exhibit an immature-appearing profile of dendritic spines
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DOI：
10.1016/j.brainres.2006.02.044
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发表时间：
2006-04-21
期刊：
影响因子：
2.9
通讯作者：
Greenough, William T.
中科院分区：
文献类型：
--
作者：
Grossman, Aaron W.;Elisseou, Nicholas M.;Greenough, William T.
脆性 X 综合征 (FXS) 是一种常见的精神发育迟滞，由功能性脆性 X 智力迟钝蛋白 (FMRP) 的缺失引起。 FXS 与树突棘的密度和长度增加以及新皮质中树突棘形态的不成熟分布特征有关。缺乏 FMRP 的小鼠（Fmr1 敲除小鼠）在新皮质中表现出类似的表型，表明 FMRP 对于树突棘的成熟和修剪很重要。对成年 Fmr1 敲除小鼠海马亚区 CA1 中高尔基染色的锥体细胞的检查显示，其脊柱比对照组更长，并且形态特征虽然与 Fmr1 敲除新皮质中描述的基本相反，但似乎同样不成熟。这一发现强烈表明 FMRP 是多个大脑区域的脊柱成熟和修剪过程所必需的，并且特定的病理学取决于细胞环境。 (c) 2006 Elsevier B.V. 保留所有权利。
Fragile X syndrome (FXS) is a common form of mental retardation caused by the absence of functional fragile X mental retardation protein (FMRP). FXS is associated with elevated density and length of dendritic spines, as well as an immature-appearing distribution profile of spine morphologies in the neocortex. Mice that lack FMRP (Fmr1 knockout mice) exhibit a similar phenotype in the neocortex, suggesting that FMRP is important for dendritic spine maturation and pruning. Examination of Golgi-stained pyramidal cells in hippocampal subfield CA1 of adult Fmr1 knockout mice reveals longer spines than controls and a morphology profile that, while essentially opposite of that described in the Fmr1 knockout neocortex, appears similarly immature. This finding strongly suggests that FMRP is required for the processes of spine maturation and pruning in multiple brain regions and that the specific pathology depends on the cellular context. (c) 2006 Elsevier B.V. All rights reserved.