帮助 关于我们

返回检索结果

Parvalbumin阳性中间神经元缺陷在精神分裂症病理机制中的作用
Roles of impaired parvalbumin positive interneurons in schizophrenic pathology

查看参考文献118篇

邓潇斐 1,2   郭建友 1 *  
文摘 精神分裂症是一种多发于青壮年的重性精神病,其原因尚不明确。经典的多巴胺缺陷理论假说在某些方面欠缺解释力;与此同时,关于Parvalbumin阳性的中间神经元(后简称PV+神经元)缺陷在精神分裂症病理机制中的作用逐渐明晰,并引起了越来越多的关注。PV+神经元在绝大部分脑区中是一种快速放电的抑制性神经元,参与了突触可塑性的调节,兴奋/抑制平衡的维持和神经发生等。而在精神分裂症中, PV+神经元的异常在患者和动物研究中都被普遍证实,并发现与NMDA受体缺陷、gamma波异常和氧化应激存在某些关联。
其他语种文摘 Schizophrenia is a severe mental disorder typically began in late adolescence or early adulthood. To date, the cause of schizophrenia remains largely unclear. The classical dopamine hypothesis of schizophrenia is now thought to be sided. Meanwhile, the involvement of impaired Parvalbumin positive interneurons (PV+ neurons) in the pathological mechanism of schizophrenia has been realized and received increasing attention. Generally, PV+ cells is a kind of inhibitory, fast-spiking interneurons, which had been demonstrated to be involved in synaptic plasticity, excitation/inhibition balance and neurogenesis. In schizophrenia, abnormal PV+ neurons has been commonly found in patients and relevant animal models., In this article, we reviewed the roles of deficits of PV+ neurons in schizophrenic pathology combined its principal phenotypes including defective NMDA receptors, abnormal gamma oscillation and oxidative stress, hoping to contribute to further investigation and development of new drugs.
来源 心理科学进展 ,2018,26(11):1992-2002 【核心库】
DOI 10.3724/SP.J.1042.2018.01992
关键词 精神分裂症 ; 中间神经元 ; NMDA受体 ; 氧化应激
地址

1. 中国科学院心理研究所, 中国科学院心理健康院重点实验室, 北京, 100101  

2. 中国科学院大学, 北京, 100049

语种 中文
文献类型 研究性论文
ISSN 1671-3710
学科 社会科学总论
基金 国家自然科学基金
文献收藏号 CSCD:6369055

参考文献 共 118 共6页

1.  Abekawa T. Prenatal exposure to an NMDA receptor antagonist, MK-801 reduces density of parvalbumin-immunoreactive GABAergic neurons in the medial prefrontal cortex and enhances phencyclidine-induced hyperlocomotion but not behavioral sensitization to methamphetamine in postpubertal rats. Psychopharmacology,2007,192(3):303-316 被引 2    
2.  Abi-Dargham A. The role of serotonin in the pathophysiology and treatment of schizophrenia. The Journal of Neuropsychiatry and Clinical Neurosciences,1997,9(1):1-17 被引 2    
3.  Aika Y. Quantitative analysis of GABA-like-immunoreactive and parvalbumin-containing neurons in the CA1 region of the rat hippocampus using a stereological method, the disector. Experimental Brain Research,1994,99(2):267-276 被引 3    
4.  Alberi L. The calcium-binding protein parvalbumin modulates the firing 1 properties of the reticular thalamic nucleus bursting neurons. Journal of Neurophysiology,2013,109(11):2827-2841 被引 1    
5.  Ali A B. Synaptic α5 subunit-containing GABAA receptors mediate IPSPs elicited by dendrite-preferring cells in rat neocortex. Cerebral Cortex,2007,18(6):1260-1271 被引 2    
6.  Barr M S. Evidence for excessive frontal evoked gamma oscillatory activity in schizophrenia during working memory. Schizophrenia Research,2010,121(1/3):146-152 被引 1    
7.  Bartos M. Synaptic mechanisms of synchronized gamma oscillations in inhibitory interneuron networks. Nature Reviews Neuroscience,2007,8(1):45-56 被引 19    
8.  Beasley C L. Parvalbumin-immunoreactive neurons are reduced in the prefrontal cortex of schizophrenics. Schizophrenia Research,1997,24(3):349-355 被引 4    
9.  Belforte J E. Postnatal NMDA receptor ablation in corticolimbic interneurons confers schizophrenia-like phenotypes. Nature Neuroscience,2010,13(1):76-83 被引 6    
10.  Behrens M M. Ketamine-induced loss of phenotype of fast-spiking interneurons is mediated by NADPH-oxidase. Science,2007,318(5856):1645-1647 被引 6    
11.  Behrens M M. Does schizophrenia arise from oxidative dysregulation of parvalbumin-interneurons in the developing cortex?. Neuropharmacology,2009,57(3):193-200 被引 1    
12.  Bezaire M J. Quantitative assessment of CA1 local circuits:Knowledge base for interneuron‐pyramidal cell connectivity. Hippocampus,2013,23(9):751-785 被引 2    
13.  Billingslea E N. Parvalbumin cell ablation of NMDA-R1 causes increased resting network excitability with associated social and self-care deficits. Neuropsychopharmacology,2014,39(7):1603-1613 被引 3    
14.  Bitanihirwe B K Y. Glutamatergic deficits and parvalbumin-containing inhibitory neurons in the prefrontal cortex in schizophrenia. BMC Psychiatry,2009,9(71):1 被引 1    
15.  Breier A. Serotonin, schizophrenia and antipsychotic drug action. Schizophrenia Research,1995,14(3):187-202 被引 3    
16.  Brenhouse H C. Nonsteroidal anti-inflammatory treatment prevents delayed effects of early life stress in rats. Biological Psychiatry,2011,70(5):434-440 被引 1    
17.  Burguiere E. Optogenetic stimulation of lateral orbitofronto-striatal pathway suppresses compulsive behaviors. Science,2013,340(6137):1243-1246 被引 5    
18.  Buzsaki G. Commissural projection to the dentate gyrus of the rat:evidence for feed-forward inhibition. Brain Research,1981,230(1/2):346-350 被引 1    
19.  Cabungcal J H. Juvenile antioxidant treatment prevents adult deficits in a developmental model of schizophrenia. Neuron,2014,83(5):1073-1084 被引 4    
20.  Cabungcal J H. Early-life insults impair parvalbumin interneurons via oxidative stress:reversal by N-acetylcysteine. Biological Psychiatry,2013,73(6):574-582 被引 2    
引证文献 1

1 姜禾佳 Parvalbumin阳性神经元在阿尔茨海默病和精神分裂症认知障碍中的作用机制 生物化学与生物物理进展,2020,47(5):418-425
被引 1

显示所有1篇文献

论文科学数据集
PlumX Metrics
相关文献

 作者相关
 关键词相关
 参考文献相关

版权所有 ©2008 中国科学院文献情报中心 制作维护:中国科学院文献情报中心
地址:北京中关村北四环西路33号 邮政编码:100190 联系电话:(010)82627496 E-mail:cscd@mail.las.ac.cn 京ICP备05002861号-4 | 京公网安备11010802043238号