Defect in normal developmental increase of the brain biogenic amine concentrations in the mecp2-null mouse
Defect in normal developmental increase of the brain biogenic amine concentrations in the mecp2-null mouse
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DOI：
10.1016/j.neulet.2005.05.056
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发表时间：
2005-09-01
影响因子：
2.5
通讯作者：
Goto, Y
中科院分区：
文献类型：
--
作者：
Ide, S;Itoh, M;Goto, Y
为了阐明Mecp 2功能障碍是否可能导致单胺能和多巴胺能系统的损害，我们通过HPLC方法测量了出生后0-42天每个年龄的3只mecp 2缺失雄性小鼠和4只对照小鼠的全脑生物胺和相关底物的浓度。出生后14天，mecp 2基因敲除小鼠体内的生物胺浓度比对照组小，出生后42天，mecp 2基因敲除小鼠体内的去甲肾上腺素、多巴胺和5-羟色胺浓度分别显著降低了25%、24%和16%。这一结果表明，Mecp 2的缺乏不会损害单胺能和多巴胺能神经元的神经发生，但会导致出生后14天这些神经元系统的后续损害。(C)2005爱思唯尔爱尔兰有限公司保留所有权利。
To clarify whether Mecp2 dysfunction may cause impairment of the monoaminergic and serotonergic systems, we measured the whole brain concentrations of biogenic amines and related substrates in three mecp2-null male mice and four control mice of each age at 0-42 postnatal days by HPLC methods. After 14 postnatal days, concentrations of biogenic amines were smaller in mecp2-null mice than those in control mice and at 42 postnatal days, norepinephrine, dopamine and serotonin concentrations in mecp2-null mice were significantly smaller by 25, 24 and 16%, respectively. This result suggested that the absence of Mecp2 does not impair the neurogenesis of monoaminergic and serotonergic neurons but causes succeeding impairment of those neuronal systems from 14 postnatal days. (C) 2005 Elsevier Ireland Ltd. All rights reserved.