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The methylazoxymethanol acetate rat model: molecular and epigenetic effect in the developing prefrontal cortex: An Editorial Highlight for 'Epigenetic mechanisms underlying NMDA receptor hypofunction in the prefrontal cortex of juvenile animals in the MAM model for schizophrenia' on page 320.乙酸甲基偶氮甲醇大鼠模型：发育中的前额叶皮质中的分子和表观遗传效应：第320页“精神分裂症MAM模型中幼年动物前额叶皮质NMDA受体功能低下的表观遗传机制”的编辑亮点
J Neurochem. 2017 Nov;143(3):264-267. doi: 10.1111/jnc.14133. Epub 2017 Sep 5.
2
Epigenetic mechanisms underlying NMDA receptor hypofunction in the prefrontal cortex of juvenile animals in the MAM model for schizophrenia.精神分裂症MAM模型中幼年动物前额叶皮质NMDA受体功能低下的表观遗传机制。
J Neurochem. 2017 Nov;143(3):320-333. doi: 10.1111/jnc.14101. Epub 2017 Sep 5.
3
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Role of the prefrontal cortex in altered hippocampal-accumbens synaptic plasticity in a developmental animal model of schizophrenia.前额叶皮层在精神分裂症发育动物模型中海马-伏隔核突触可塑性改变中的作用。
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Abnormalities in behaviour, histology and prefrontal cortical gene expression profiles relevant to schizophrenia in embryonic day 17 MAM-Exposed C57BL/6 mice.胚胎期 17 天 MAM 暴露的 C57BL/6 小鼠与精神分裂症相关的行为、组织学和前额叶皮质基因表达谱的异常。
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Gestational methylazoxymethanol acetate treatment impairs select cognitive functions: parallels to schizophrenia.孕期乙酸甲基偶氮甲醇治疗会损害特定认知功能：与精神分裂症的相似之处。
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Biochemical and cognitive impairments observed in animal models of schizophrenia induced by prenatal stress paradigm or methylazoxymethanol acetate administration.在产前应激范式或给予乙酸甲基氧化偶氮甲醇诱导的精神分裂症动物模型中观察到的生化和认知障碍。
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A neurobehavioral systems analysis of adult rats exposed to methylazoxymethanol acetate on E17: implications for the neuropathology of schizophrenia.对在胚胎第17天暴露于乙酸甲基氧化偶氮甲醇的成年大鼠进行神经行为系统分析：对精神分裂症神经病理学的启示
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Preclinical characterization of AMPA receptor potentiator TAK-137 as a therapeutic drug for schizophrenia.AMPA 受体增强剂 TAK-137 治疗精神分裂症的临床前特征。
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本文引用的文献

1
Epigenetic mechanisms underlying NMDA receptor hypofunction in the prefrontal cortex of juvenile animals in the MAM model for schizophrenia.精神分裂症MAM模型中幼年动物前额叶皮质NMDA受体功能低下的表观遗传机制。
J Neurochem. 2017 Nov;143(3):320-333. doi: 10.1111/jnc.14101. Epub 2017 Sep 5.
2
The emerging field of epigenetics in neurodegeneration and neuroprotection.神经退行性变与神经保护领域中新兴的表观遗传学
Nat Rev Neurosci. 2017 May 18;18(6):347-361. doi: 10.1038/nrn.2017.46.
3
Adolescent Stress as a Driving Factor for Schizophrenia Development-A Basic Science Perspective.青少年压力作为精神分裂症发病的驱动因素——基础科学视角
Schizophr Bull. 2017 May 1;43(3):486-489. doi: 10.1093/schbul/sbx033.
4
Adolescence as a period of vulnerability and intervention in schizophrenia: Insights from the MAM model.青少年期作为精神分裂症的易患期及干预阶段：来自MAM模型的见解
Neurosci Biobehav Rev. 2016 Nov;70:260-270. doi: 10.1016/j.neubiorev.2016.05.030. Epub 2016 May 24.
5
Altering the course of schizophrenia: progress and perspectives.改变精神分裂症的病程：进展与展望。
Nat Rev Drug Discov. 2016 Jul;15(7):485-515. doi: 10.1038/nrd.2016.28. Epub 2016 Mar 4.
6
Schizophrenia-Like Phenotype Inherited by the F2 Generation of a Gestational Disruption Model of Schizophrenia.精神分裂症妊娠中断模型F2代遗传的精神分裂症样表型
Neuropsychopharmacology. 2016 Jan;41(2):477-86. doi: 10.1038/npp.2015.169. Epub 2015 Jun 12.
7
Translating the MAM model of psychosis to humans.将精神病的MAM模型应用于人类。
Trends Neurosci. 2015 Mar;38(3):129-38. doi: 10.1016/j.tins.2014.12.005. Epub 2014 Dec 30.
8
Epigenetic mechanisms in schizophrenia.精神分裂症中的表观遗传机制。
Dialogues Clin Neurosci. 2014 Sep;16(3):405-17. doi: 10.31887/DCNS.2014.16.3/sakbarian.
9
The glutamate hypothesis of schizophrenia: evidence from human brain tissue studies.精神分裂症的谷氨酸假说：来自人脑组织研究的证据。
Ann N Y Acad Sci. 2015 Mar;1338(1):38-57. doi: 10.1111/nyas.12547. Epub 2014 Oct 14.
10
NMDA receptor subunit diversity: impact on receptor properties, synaptic plasticity and disease.NMDA 受体亚单位多样性：对受体特性、突触可塑性和疾病的影响。
Nat Rev Neurosci. 2013 Jun;14(6):383-400. doi: 10.1038/nrn3504.

乙酸甲基偶氮甲醇大鼠模型：发育中的前额叶皮质中的分子和表观遗传效应：第320页“精神分裂症MAM模型中幼年动物前额叶皮质NMDA受体功能低下的表观遗传机制”的编辑亮点

The methylazoxymethanol acetate rat model: molecular and epigenetic effect in the developing prefrontal cortex: An Editorial Highlight for 'Epigenetic mechanisms underlying NMDA receptor hypofunction in the prefrontal cortex of juvenile animals in the MAM model for schizophrenia' on page 320.

作者信息

Zhu Xiyu, Gomes Felipe V, Grace Anthony A

机构信息

Departments of Neuroscience, Psychiatry and Psychology, University of Pittsburgh, Pittsburgh, PA, USA.

出版信息

J Neurochem. 2017 Nov;143(3):264-267. doi: 10.1111/jnc.14133. Epub 2017 Sep 5.

DOI:10.1111/jnc.14133
PMID:28872674
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5679231/
Abstract

This Editorial highlights an article by Gulchina and colleagues in the current issue of the Journal of Neurochemistry, in which the authors describe molecular and epigenetic changes in the developing prefrontal cortex of the rats exposed to methylazoxymethanol acetate (MAM). They found an NMDAR hypofunction present in the prefrontal cortex of juvenile MAM rats which was associated with abnormal epigenetic regulation of the Grin2b gene. These changes may be related to early cognitive impairments observed in MAM rats and schizophrenia patients.

摘要

本社论重点介绍了古尔奇娜及其同事在本期《神经化学杂志》上发表的一篇文章，作者在文中描述了暴露于乙酸甲基偶氮甲醇（MAM）的大鼠发育中的前额叶皮质的分子和表观遗传变化。他们发现幼年MAM大鼠的前额叶皮质存在NMDAR功能减退，这与Grin2b基因的异常表观遗传调控有关。这些变化可能与在MAM大鼠和精神分裂症患者中观察到的早期认知障碍有关。