Utility of genetically modified mice for understanding the neurobiology of substance use disorders.
Utility of genetically modified mice for understanding the neurobiology of substance use disorders.
复制标题
DOI：
10.1007/s00439-011-1129-z
复制
发表时间：
2012-06
期刊：
影响因子：
5.3
通讯作者：
Kenny PJ
中科院分区：
文献类型：
--
作者：
Fowler CD;Kenny PJ
我们修改小鼠基因组的能力的进步增强了我们对药物使用和滥用背后的成瘾相关行为的遗传和神经生物学机制的理解。这些实验诱导的操作允许在特定细胞群体和特定发育时期内对基因表达进行更大的空间和时间特异性修饰。在这篇综述中，我们考虑了目前用于理解成瘾方面的小鼠遗传模型系统，并强调了与物质使用和滥用相关的重大概念进展。本文综述的小鼠模型包括常规敲除和敲入、条件敲除、转基因、诱导转基因、适合光遗传控制离散神经元群体的小鼠和表型选择小鼠。通过建立人类遗传发现和小鼠基因组操作之间的互惠调查关系，可以更好地了解成瘾的离散神经机制，这可能为开发和验证治疗药物滥用障碍的新疗法提供坚实的基础。
Advances in our ability to modify the mouse genome have enhanced our understanding of the genetic and neurobiological mechanisms contributing to addiction-related behaviors underlying substance use and abuse. These experimentally induced manipulations permit greater spatial and temporal specificity for modification of gene expression within specific cellular populations and during select developmental time periods. In this review, we consider the current mouse genetic model systems that have been employed to understand aspects of addiction and highlight significant conceptual advances achieved related to substance use and abuse. The mouse models reviewed herein include conventional knockout and knockin, conditional knockout, transgenic, inducible transgenic, mice suitable for optogenetic control of discrete neuronal populations, and phenotype-selected mice. By establishing a reciprocal investigatory relationship between genetic findings in humans and genomic manipulations in mice, a far better understanding of the discrete neuromechanisms underlying addiction can be achieved, which is likely to provide a strong foundation for developing and validating novel therapeutics for the treatment of substance abuse disorders.
登录
查看更多内容
纹状体培养基神经元的功能连接组。
DOI：
10.1523/jneurosci.3833-10.2011
发表时间：
2011-01-26
期刊：
The Journal of neuroscience : the official journal of the Society for Neuroscience
影响因子：
--
作者：
Chuhma N;Tanaka KF;Hen R;Rayport S
通讯作者：
Rayport S
DOI：
10.1073/pnas.1101791108
发表时间：
2011-07-19
影响因子：
11.1
作者：
Chen, Alice A.;Thomas, David K.;Bhatia, Sangeeta N.
通讯作者：
Bhatia, Sangeeta N.
影响因子：
--
作者：
Brody, Arthur L.;Mandelkern, Mark A.;Mukhin, Alexey G.
通讯作者：
Mukhin, Alexey G.
DOI：
10.1523/jneurosci.2246-11.2011
发表时间：
2011-07-27
期刊：
The Journal of neuroscience : the official journal of the Society for Neuroscience
影响因子：
--
作者：
Adamantidis AR;Tsai HC;Boutrel B;Zhang F;Stuber GD;Budygin EA;Touriño C;Bonci A;Deisseroth K;de Lecea L
通讯作者：
de Lecea L
影响因子：
5.3
作者：
Corbille, Anne-Gaelle;Valjent, Emmanuel;Girault, Jean-Antoine
通讯作者：
Girault, Jean-Antoine