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纹状体转录组变化与药物诱导的重复性行为有关。

Striatal transcriptome changes linked to drug-induced repetitive behaviors.

机构信息

McGovern Institute for Brain Research, The Massachusetts Institute of Technology, Cambridge, MA, USA.

Department of Brain and Cognitive Sciences, The Massachusetts Institute of Technology, Cambridge, MA, USA.

出版信息

Eur J Neurosci. 2021 Apr;53(8):2450-2468. doi: 10.1111/ejn.15116. Epub 2021 Mar 23.

Abstract

Disruptive or excessive repetitive motor patterns (stereotypies) are cardinal symptoms in numerous neuropsychiatric disorders. Stereotypies are also evoked by psychomotor stimulants such as amphetamine. The acquisition of motor sequences is paralleled by changes in activity patterns in the striatum, and stereotypies have been linked to abnormal plasticity in these reinforcement-related circuits. Here, we designed experiments in mice to identify transcriptomic changes that underlie striatal plasticity occurring alongside the development of drug-induced stereotypic behavior. We identified three schedules of amphetamine treatment inducing different degrees of stereotypy and used bulk RNAseq to compare striatal gene expression changes among groups of mice treated with the different drug-dose schedules and vehicle-treated, cage-mate controls. Mice were identified as naïve, sensitized, or tolerant to drug-induced stereotypy. All drug-treated groups exhibited expression changes in genes that encode members of the extracellular signal-regulated kinase (ERK) cascades known to regulate psychomotor stimulant responses. In the sensitized group with the most prolonged stereotypy, we found dysregulation of 20 genes that were not changed in other groups. Gene set enrichment analysis indicated highly significant overlap with genes regulated by neuregulin 1 (Nrg1). Nrg1 is known to be a schizophrenia and autism susceptibility gene that encodes a ligand for Erb-B receptors, which are involved in neuronal migration, myelination, and cell survival, including that of dopamine-containing neurons. Stimulant abuse is a risk factor for schizophrenia onset, and these two disorders share behavioral stereotypy phenotypes. Our results raise the possibility that drug-induced sensitization of the Nrg1 signaling pathway might underlie these links.

摘要

在许多神经精神疾病中,异常或过度重复的运动模式(刻板行为)是主要症状。精神运动兴奋剂,如安非他命,也会引起刻板行为。运动序列的获得伴随着纹状体活动模式的变化,刻板行为与这些与强化相关的回路中的异常可塑性有关。在这里,我们在小鼠中设计了实验,以确定与药物诱导的刻板行为发展相伴发生的纹状体可塑性的转录组变化基础。我们确定了三种安非他命处理方案,这些方案会引起不同程度的刻板行为,并使用 bulk RNAseq 来比较用不同药物剂量方案和载体处理的、笼内对照的小鼠的纹状体基因表达变化。将小鼠鉴定为对药物诱导的刻板行为呈幼稚、敏感或耐受状态。所有药物处理组都表现出编码细胞外信号调节激酶 (ERK) 级联的成员的基因表达变化,这些基因已知可调节精神运动兴奋剂反应。在具有最持久刻板行为的敏感化组中,我们发现 20 个基因失调,而其他组没有变化。基因集富集分析表明与神经调节蛋白 1 (Nrg1) 调节的基因高度重叠。Nrg1 是精神分裂症和自闭症易感基因,编码 Erb-B 受体的配体,该受体参与神经元迁移、髓鞘形成和细胞存活,包括多巴胺能神经元的存活。兴奋剂滥用是精神分裂症发病的一个风险因素,而这两种疾病具有行为刻板行为表型。我们的结果提出了一种可能性,即 Nrg1 信号通路的药物诱导敏感可能是这些联系的基础。

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