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本文引用的文献

1
Epigenetic transgenerational inheritance of altered stress responses.表观遗传跨代传递改变的应激反应。
Proc Natl Acad Sci U S A. 2012 Jun 5;109(23):9143-8. doi: 10.1073/pnas.1118514109. Epub 2012 May 21.
2
Haploinsufficiency of the E3 ubiquitin ligase C-terminus of heat shock cognate 70 interacting protein (CHIP) produces specific behavioral impairments.E3 泛素连接酶热休克同源物 70 相互作用蛋白(CHIP)C 端单倍不足导致特定的行为障碍。
PLoS One. 2012;7(5):e36340. doi: 10.1371/journal.pone.0036340. Epub 2012 May 11.
3
Development of hyperactivity and anxiety responses in dopamine transporter-deficient mice.多巴胺转运体缺陷型小鼠多动和焦虑反应的发展。
Dev Neurosci. 2012;34(2-3):250-7. doi: 10.1159/000336824. Epub 2012 May 8.
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Paternal transmission of stress-induced pathologies.应激相关疾病的父系传递。
Biol Psychiatry. 2011 Sep 1;70(5):408-14. doi: 10.1016/j.biopsych.2011.05.005. Epub 2011 Jun 16.
5
Loss of Thr286 phosphorylation disrupts synaptic CaMKIIα targeting, NMDAR activity and behavior in pre-adolescent mice.Thr286 磷酸化缺失破坏了青春期前小鼠突触 CaMKIIα 的靶向定位、NMDAR 活性和行为。
Mol Cell Neurosci. 2011 Aug;47(4):286-92. doi: 10.1016/j.mcn.2011.05.006. Epub 2011 May 24.
6
Paternal occupational exposures and the risk of congenital malformations--a case-control study.父亲职业暴露与先天性畸形风险的病例对照研究。
Int J Occup Med Environ Health. 2011 Jun;24(2):218-27. doi: 10.2478/s13382-011-0019-x. Epub 2011 May 7.
7
Autism and increased paternal age related changes in global levels of gene expression regulation.自闭症与父代年龄增加相关的基因表达调控的全球水平变化。
PLoS One. 2011 Feb 17;6(2):e16715. doi: 10.1371/journal.pone.0016715.
8
Translational issues for prenatal cocaine studies and the role of environment.产前可卡因研究的转化问题与环境的作用。
Neurotoxicol Teratol. 2011 Jan-Feb;33(1):9-16. doi: 10.1016/j.ntt.2010.06.007. Epub 2010 Jun 30.
9
Ascorbic acid attenuates scopolamine-induced spatial learning deficits in the water maze.抗坏血酸可减轻东莨菪碱诱导的水迷宫空间学习障碍。
Behav Brain Res. 2009 Dec 28;205(2):550-8. doi: 10.1016/j.bbr.2009.08.017. Epub 2009 Aug 22.
10
Paternal transmission of complex phenotypes in inbred mice.近交系小鼠复杂表型的父系传递。
Biol Psychiatry. 2009 Dec 1;66(11):1061-6. doi: 10.1016/j.biopsych.2009.05.026. Epub 2009 Jul 3.

父代可卡因暴露产生的微妙生物行为效应。

Subtle biobehavioral effects produced by paternal cocaine exposure.

机构信息

Department of Pharmacology, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA.

出版信息

Synapse. 2012 Oct;66(10):902-8. doi: 10.1002/syn.21582. Epub 2012 Jul 27.

DOI:10.1002/syn.21582
PMID:22807092
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3432506/
Abstract

Despite the increased prevalence of cocaine use and abuse in males when compared with females, possible effects of paternal cocaine exposure on biobehavioral development have received little attention. We therefore exposed male mice to cocaine (20 mg/kg, i.p.) or vehicle for 10 weeks and then used those mice as sires. We then behaviorally phenotyped the F1 offspring to assess the consequences of paternal cocaine exposure on brain function. We report the presence of a subtle but significant increase in immobility in the tail suspension test, a measure of behavioral depression, following paternal cocaine. Body weight was also significantly decreased in paternal cocaine-exposed offspring. Other aspects of neurobehavioral function, including locomotor activity, anxiety, and learning and memory, were not affected by paternal cocaine history. These data suggest alterations in brain systems and/or circuitry underlying mood regulation in the offspring of cocaine-using fathers. Synapse 2012. © 2012 Wiley Periodicals, Inc.

摘要

尽管与女性相比,男性可卡因使用和滥用的情况更为普遍,但父代可卡因暴露对生物行为发育的可能影响却很少受到关注。因此,我们让雄性老鼠接受可卡因(20mg/kg,腹腔注射)或载体 10 周,然后让这些老鼠作为父鼠。然后,我们对 F1 后代进行行为表型分析,以评估父代可卡因暴露对大脑功能的影响。我们报告说,在尾巴悬挂测试中,行为抑郁的一种衡量标准,即不动性,在雄性可卡因暴露后出现了轻微但显著的增加。父代可卡因暴露的后代的体重也显著下降。神经行为功能的其他方面,包括运动活动、焦虑和学习记忆,不受父代可卡因史的影响。这些数据表明,在使用可卡因的父亲的后代中,与情绪调节相关的大脑系统和/或电路发生了改变。Synapse 2012。©2012 Wiley Periodicals, Inc.