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Time to abandon the bio-bio-bio model of psychosis: Exploring the epigenetic and psychological mechanisms by which adverse life events lead to psychotic symptoms.是时候摒弃精神病的生物-生物-生物模型了:探索不良生活事件导致精神病症状的表观遗传和心理机制。
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2
Modeling the positive symptoms of schizophrenia in genetically modified mice: pharmacology and methodology aspects.建模遗传修饰小鼠的精神分裂症阳性症状:药理学和方法学方面。
Schizophr Bull. 2010 Mar;36(2):246-70. doi: 10.1093/schbul/sbp132. Epub 2009 Nov 9.
3
The interaction between genetics and epidemiology: the puzzle and its pieces.
Epidemiol Psichiatr Soc. 2009 Apr-Jun;18(2):77-80.
4
Breaking the gene barrier in schizophrenia.突破精神分裂症的基因障碍。
Nat Med. 2009 May;15(5):488-90. doi: 10.1038/nm0509-488.
5
A primate-specific, brain isoform of KCNH2 affects cortical physiology, cognition, neuronal repolarization and risk of schizophrenia.KCNH2的一种灵长类动物特有的脑亚型影响皮层生理学、认知、神经元复极化和精神分裂症风险。
Nat Med. 2009 May;15(5):509-18. doi: 10.1038/nm.1962. Epub 2009 May 3.
6
The dopamine hypothesis of schizophrenia: version III--the final common pathway.精神分裂症的多巴胺假说:第三版——最终共同通路
Schizophr Bull. 2009 May;35(3):549-62. doi: 10.1093/schbul/sbp006. Epub 2009 Mar 26.
7
Transcription factor Gbx2 acts cell-nonautonomously to regulate the formation of lineage-restriction boundaries of the thalamus.转录因子Gbx2通过非细胞自主方式调节丘脑谱系限制边界的形成。
Development. 2009 Apr;136(8):1317-26. doi: 10.1242/dev.030510. Epub 2009 Mar 11.
8
Expressions of genes encoding drug-metabolizing enzymes are altered after sevoflurane, isoflurane, propofol or dexmedetomidine anesthesia.七氟烷、异氟烷、丙泊酚或右美托咪定麻醉后,编码药物代谢酶的基因表达会发生改变。
Biomed Res. 2009 Feb;30(1):17-24. doi: 10.2220/biomedres.30.17.
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Developmentally regulated and thalamus-selective induction of leiomodin2 gene by a schizophrenomimetic, phencyclidine, in the rat.在大鼠中,一种拟精神分裂症药物苯环利定对平滑肌肌动蛋白调节蛋白2基因进行发育调控且具有丘脑选择性诱导作用。
Int J Neuropsychopharmacol. 2009 Sep;12(8):1111-26. doi: 10.1017/S1461145709009997. Epub 2009 Mar 2.
10
Contracting schizophrenia: lessons from the influenza epidemic of 1918-1919.患精神分裂症:从1918 - 1919年流感大流行中吸取的教训
JAMA. 2009 Jan 21;301(3):324-6. doi: 10.1001/jama.2008.980.

精神分裂症啮齿动物模型中的基因表达谱分析。

Gene expression profiling in rodent models for schizophrenia.

机构信息

Department of Molecular Animal Physiology, Donders Institute for Brain, Cognition and Behaviour, Centre for Neuroscience & Nijmegen Centre for Molecular Life Sciences (NCMLS), Faculty of Science, Radboud University Nijmegen, 6525 GA, Nijmegen, The Netherlands.

出版信息

Curr Neuropharmacol. 2010 Dec;8(4):382-93. doi: 10.2174/157015910793358132.

DOI:10.2174/157015910793358132
PMID:21629445
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3080594/
Abstract

The complex neurodevelopmental disorder schizophrenia is thought to be induced by an interaction between predisposing genes and environmental stressors. In order to get a better insight into the aetiology of this complex disorder, animal models have been developed. In this review, we summarize mRNA expression profiling studies on neurodevelopmental, pharmacological and genetic animal models for schizophrenia. We discuss parallels and contradictions among these studies, and propose strategies for future research.

摘要

精神分裂症是一种复杂的神经发育障碍,据认为是由易感基因和环境应激源相互作用引起的。为了更好地了解这种复杂疾病的病因,已经开发了动物模型。在这篇综述中,我们总结了神经发育、药理学和遗传精神分裂症动物模型的 mRNA 表达谱研究。我们讨论了这些研究之间的相似之处和矛盾之处,并提出了未来研究的策略。