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Neuron:自闭症相关蛋白在成瘾行为中发挥重要作用

来源:生物谷 2014-05-11 20:50

2014年5月11日讯 /生物谷BIOON/--发表在最新一期Neuron杂志上的一篇论文中,McLean医院研究人员报告说,对大脑正常发育至关重要的基因,同时也是与自闭症相关的基因,在成瘾相关行为中也发挥关键作用。

在实验室中,研究人员调查吸毒成瘾背后的脑机制,Christopher Cowan博士解释说:药物滥用导致大脑变化,导致成瘾,通过发现大脑中控制毒瘾发展的分子,我们希望找出成瘾新的治疗方法。

Cowan实验室团队用动物模型来表明脆性X智力迟钝蛋白或FMRP在成瘾相关行为发展中起着关键作用。FMRP也是在脆性X综合征中缺失的蛋白质,是引起孤独症和智力残疾的基因。与其在脑功能的重要作用一致,研究小组发现,可卡因利用FMRP以推动成瘾相关行为的大脑变化。

Cowan解释说,正常发育过程中,FMRP控制大脑连接的重塑和力量。他们目前的研究结果表明,FMRP在反复暴露于可卡因之后,大脑连接的改变中起到至关重要的作用。

通过更好地了解FMRP在这个过程中的作用,可能有一天能够提出有效的治疗方案阻止或逆转这些大脑变化。(生物谷Bioon.com)

Fragile X Mental Retardation Protein Regulates Synaptic and Behavioral Plasticity to Repeated Cocaine Administration

Laura N. Smith, Jakub P. Jedynak, Miles R. Fontenot, Carly F. Hale, Karen C. Dietz, Makoto Taniguchi, Feba S. Thomas, Benjamin C. Zirlin, Shari G. Birnbaum, Kimberly M. Huber, Mark J. Thomas, Christopher W.

Repeated cocaine exposure causes persistent, maladaptive alterations in brain and behavior, and hope for effective therapeutics lies in understanding these processes. We describe here an essential role for fragile X mental retardation protein (FMRP), an RNA-binding protein and regulator of dendritic protein synthesis, in cocaine conditioned place preference, behavioral sensitization, and motor stereotypy. Cocaine reward deficits in FMRP-deficient mice stem from elevated mGluR5 (or GRM5) function, similar to a subset of fragile X symptoms, and do not extend to natural reward. We find that FMRP functions in the adult nucleus accumbens (NAc), a critical addiction-related brain region, to mediate behavioral sensitization but not cocaine reward. FMRP-deficient mice also exhibit several abnormalities in NAc medium spiny neurons, including reduced presynaptic function and premature changes in dendritic morphology and glutamatergic neurotransmission following repeated cocaine treatment. Together, our findings reveal FMRP as a critical mediator of cocaine-induced behavioral and synaptic plasticity.

 

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