压力与双相情感障碍

R. McCarty
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引用次数: 0

摘要

双相情感障碍(BD)的动物模型应该捕捉情绪状态从躁狂到抑郁的转换,反之亦然。脑内多巴胺信号通路,包括多巴胺转运蛋白的变化,一直是许多双相障碍动物模型关注的焦点。人类双相障碍的另一个方面反映在症状发作的昼夜节律和季节变化上。其他双相障碍的动物模型包括梅什金和麦迪逊小鼠品系,这两种小鼠都表现出类似躁狂的行为,用锂或丙戊酸治疗后会逆转。另一种实验方法是操纵生物钟基因,并检查对多巴胺信号和行为的影响。最后,在实验室小鼠中对双相障碍风险基因的操作提高了我们对情绪状态极端改变的分子机制的理解。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Stress and Bipolar Disorder
Animal models of bipolar disorder (BD) should capture the switching of mood states from mania to depression and vice versa. Dopamine signaling pathways in brain, including variations in the dopamine transporter protein, have been a focus of many animal models of BD. Another aspect of BD in humans is reflected in circadian and seasonal changes in onset of symptoms. Other animal models of BD include the Myshkin and Madison mouse strains, both of which display mania-like behavior that is reversed by treatment with lithium or valproic acid. Another experimental approach has been to manipulate circadian clock genes and examine effects on dopamine signaling and behavior. Finally, manipulations of risk genes for BD in laboratory mice have advanced our understanding of the molecular mechanisms involved in extreme alterations in mood state.
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