Abnormal behavioral phenotypes of serotonin transporter knockout mice: Parallels with human anxiety and depression
Abnormal behavioral phenotypes of serotonin transporter knockout mice: Parallels with human anxiety and depression
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DOI：
10.1016/j.biopsych.2003.09.003
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发表时间：
2003-11-15
影响因子：
10.6
通讯作者：
Crawley, JN
中科院分区：
文献类型：
--
作者：
Holmes, A;Murphy, DL;Crawley, JN
血清素转运体的遗传变异与抑郁和焦虑之间存在联系的证据促使产生了血清素转运体敲除小鼠。敲除中5-羟色胺再摄取功能的丧失导致细胞外5-羟色胺清除率降低以及5-羟色胺神经元放电和受体功能的相关改变。敲除的行为表型功能揭示了遗传背景相关的异常，包括焦虑样行为增加，攻击性降低和过度的压力反应。正在进行的研究集中在确定环境，遗传和发育因素相互作用的htt突变产生这些异常。5-羟色胺转运体无效突变小鼠为研究5-羟色胺转运体功能的遗传变异如何影响神经精神疾病的风险提供了模型系统。Biol Psychiatry 2003; 54：953-959（C）2003生物精神病学学会
Evidence of a link between genetic variation of the serotonin transporter and depression and anxiety prompted the generation of serotonin transporter knockout mice. Loss of serotonin reuptake function in knockouts causes reduced clearance of extracellular serotonin and associated alterations in serotonin neuronal firing and receptor function. Behavioral phenotyping function in knock-outs revealed genetic background-related abnormalities, including increased anxiety-like behaviors, reduced aggression, and exaggerated stress responses. Ongoing studies focus on identifying environmental, genetic, and developmental factors interacting with the htt mutation to produce these abnormalities. Serotonin transporter null mutant mice provide a model system to study how genetic variation in serotonin transporter function affects risk for neuropsychiatric disease. Biol Psychiatry 2003; 54:953-959 (C) 2003 Society of Biological Psychiatry