神经增生在神经性毒物诱导的帕金森病动物模型中的研究进展

doi:10.16098/j.issn.0529-1356.2017.05.020

解剖学报 ›› 2017, Vol. 48 ›› Issue (5): 610-616.doi: 10.16098/j.issn.0529-1356.2017.05.020

神经增生在神经性毒物诱导的帕金森病动物模型中的研究进展

谢明琦^1,2陈治池^1,2王彤彤^1,2周翔³黄厚菊^2,4 戚双双⁵廖敏^2,4孙臣友^1,2*

1.温州医科大学基础医学院人体解剖学教研室，浙江温州 325035; 2.温州医科大学基础医学院神经科学研究所，浙江温州 325035; 3.温州医科大学第二临床医学院口腔科，浙江温州 325035; 4.温州医科大学基础医学院组织学胚胎学教研室，浙江温州 325035; 5.温州医科大学附属第二人民医院药剂科，浙江温州 325000

收稿日期:2016-10-24 修回日期:2016-11-24 出版日期:2017-10-06 发布日期:2017-10-06
通讯作者: 孙臣友 E-mail:sunchenyou1972@aliyun.com
基金资助:
别孕烯醇酮促进PD小鼠多巴胺能神经元新生的作用及机制;Al|opregnanolone诱导AD小鼠黑质多巴胺能神经元增多的机制研究;CD133追综APα诱导的6-OHDA PD小鼠新生多巴胺能神经元起源的应用研究;CD133+室管膜细胞的建立及追踪新生多巴胶能神经元起源的应用研究

Current status of neurogenesis in neurotoxin-induced animal models for Parkinson’s disease

XIE Ming-qi ^1,2CHEN Zhi-chi ^{1, 2} WANG Tong-tong ^{1, 2} ZHOU Xiang³ HUANG Hou-ju ^2,4 QI Shuang-shuang⁵ LIAO Min ^{2, 4} SUN Chen-you ^{1, 2*}

1.Department of Anatomy, School of Basic Medical Sciences, Wenzhou Medical University, Zhejiang Wenzhou 325035, China; 2.Institute of Neuroscience, School of Basic Medical Sciences, Wenzhou Medical University, Zhejiang Wenzhou 325035, China; 3.the Second Clinical Medical College, Wenzhou Medical University, Zhejiang Wenzhou 325035, China; 4.Department of Histology and Embryology, School of Basic Medical Sciences, Wenzhou Medical University, Zhejiang Wenzhou 325035, China; 5.Department of Pharmacy, Second Affiliated Hospital of Wenzhou Medical University, Zhejiang Wenzhou 325000, China

Received:2016-10-24 Revised:2016-11-24 Online:2017-10-06 Published:2017-10-06
Contact: SUN Chen-you E-mail:sunchenyou1972@aliyun.com

摘要/Abstract

摘要：

帕金森病（PD）动物模型对理解该病病因、发病机制以及检测新的治疗方案具有重要作用。成年哺乳动物脑中内源性神经增生的发现为基于细胞方法治疗神经退行性疾病，如PD，提供了新的探索方向。虽然神经性毒物诱导帕金森病动物模型脑中存在的内源性神经增生引起人们广泛的兴趣，但神经干细胞是否会迁移至受损脑区并促进神经性毒物损伤后成年大脑内减少的多巴胺能神经元数目再增依然存在着争议。我们通过综述关于神经性毒物损伤所致的PD动物模型中神经增生的文献，旨在加深神经增生在神经性毒物诱导的PD动物模型中作用的理解。

关键词: 帕金森病, 神经性毒物, 神经干细胞, 神经增生, 动物模型

Abstract:

The animal model of Parkinson’s disease (PD) plays an important role in understanding its etiology, pathogenesis and detection of new treatment regimens. The discovery of endogenous neurogenesis in the adult mammalian brain provides a new direction for the therapy of neurodegenerative diseases, such as PD, based on cellular approaches. Although a lot of attention has been focused on neurotoxininduced endogenous neurogenesis in the brain of animal models for PD, it remains controversial whether neural stem cells migrate to the damaged brain region and promote the repopulation of reduced dopaminergic neurons in adult neurotoxic injured animals. In this paper, we review various literatures on neurogenesis in neurotoxininduced animal models for PD, aiming to deepen the understanding of the role of neurogenesis in neurotoxicity-induced animal models for PD.

Key words: Parkinson’s disease, Neurotoxin, Neural stem cell, Neurogenesis, Animal model

谢明琦陈治池王彤彤周翔黄厚菊戚双双廖敏孙臣友. 神经增生在神经性毒物诱导的帕金森病动物模型中的研究进展[J]. 解剖学报, 2017, 48(5): 610-616.

XIE Ming-qi CHEN Zhi-chi WANG Tong-tong ZHOU Xiang HUANG Hou-ju QI Shuang-shuang LIAO Min SUN Chen-you. Current status of neurogenesis in neurotoxin-induced animal models for Parkinson’s disease[J]. Acta Anatomica Sinica, 2017, 48(5): 610-616.

参考文献

［1］Fahn S. The medical treatment of Parkinson’s disease from James Parkinson to George Cotzias［J］. Mov Disord, 2015, 30(1):4-18.

［2］Przedborski S, Vila M. The 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine mouse model: a tool to explore the pathogenesis of Parkinson’s disease.［J］. Ann N Y Acad Sci, 2003, 991:189-198.

［3］Nakayama H, Ito T, Shibui Y, et al. Neurotoxicity of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) as a Parkinson’s disease model［J］. Hand Book of Neurotoxicity, 2014,933-951.

［4］Jr DER. Animal Models of Movement Disordes ［M］. Clifton: Humana Press, 2011: 41-436.

［5］Delaville C, Cruz AV, Mccoy AJ, et al. Oscillatory activity in basal ganglia and motor cortex in an awake behaving rodent model of Parkinson’s disease［J］. Basal Ganglia, 2014, 3(4):221-227.

［6］Zhao C, Deng W, Gage FH. Mechanisms and functional implications of adult neurogenesis［J］. Cell, 2008, 132(4): 645-660.

［7］Olude AM, Olopade JO, Ihunwo AO. Adult neurogenesis in the African giant rat (Cricetomysgambianus, waterhouse)［J］. Metab Brain Dis, 2014, 29(3):857-866.

［8］Perera TD,Dwork AJ,Keegan KA, et al. Necessity of hippocampal neurogenesis for the therapeutic action of antidepressants in adult nonhuman primates［J］. PLoS One, 2011, 6(4): e17600.

［9］Gulati A. Understanding neurogenesis in the adult human brain［J］. Indian J Pharmacol, 2015, 47(6):583-584.

［10］Aligholi H, Hassanzadeh G, Azari H, et al. A new and safe method for stereotactically harvesting neural stem/progenitor cells from the adult rat subventricular zone［J］. J Neurosci Methods, 2014, 225(2):81-89.

［11］He XJ, Nakayama H. Neurogenesis in neurotoxin-induced animal models for Parkinson’s disease—a review of the current status［J］. J Toxicol Pathol, 2009, 22(2):101-108.

［12］Berge SA, Middeldorp J, Zhang CE, et al. Longterm quiescent cells in the aged human subventricular neurogenic system specifically express GFAP-δ［J］. Aging Cell, 2010, 9(3):313-326.

［13］Kishimoto N, Alfaro-Cervello C, Shimizu K, et al. Migration of neuronal precursors from the telencephalic ventricular zone into the olfactory bulb in adult zebrafish［J］. J Comp Neurol, 2011, 519(17):3549-3565.

［14］Chen R, Lin C, You Y, et al. Characterization of immature and mature 5-hydroxytryptamine 3A receptor-expressing cells within the adult SVZ-RMS-OB system［J］. Neuroscience, 2012, 227(1):180-190.

［15］Puverel S, Nakatani H, Parras C, et al. Prokineticin receptor 2 expression identifies migrating neuroblasts and their subventricular zone transient-amplifying progenitors in adult mice［J］. J Comp Neurol, 2008, 512(2):232-242.

［16］Mao W, Xin Y, Qin J, et al. CXCL12/CXCR4 axis improves migration of neuroblasts along corpus callosum by stimulating MMP-2 secretion after traumatic brain injury in rats［J］. Neurochem Res, 2016, 41(6): 1315-1322.

［17］Wang C, Liu F, Liu YY, et al. Identification and characterization of neuroblasts in the subventricular zone and rostral migratory stream of the adult human brain［J］. Cell Res, 2011, 21(11):1534-1550.

［18］Fink CC, Bayer KU, Myers JW, et al. Developmental dysregulation of adult neurogenesis［J］. Eur J Neurosci, 2011, 33(6):1115-1122.

［19］Yang P, Zhang J, Shi H, et al. Developmental profile of neurogenesis in prenatal human hippocampus: an immunohistochemical study［J］. Int J Dev Neurosci, 2014, 38:1-9.

［20］Brus M, Keller M, Lévy F. Temporal features of adult neurogenesis: differences and similarities across mammalian species.［J］. Front Neurosci, 2013, 7(7):135.

［21］Yamaguchi M, Seki T, Imayoshi I, et al. Neural stem cells and neuro/gliogenesis in the central nervous system: understanding the structural and functional plasticity of the developing, mature, and diseased brain［J］. J Phys Sci, 2015, 66(3):1-10.

［22］Kazanis I. Can adult neural stem cells create new brains? Plasticity in the adult mammalian neurogenic niches: realities and expectations in the era of regenerative biology［J］. Neuroscientist, 2011, 18(1):15-27.

［23］Marxreiter F, Regensburger M, Winkler J. Adult neurogenesis in Parkinson’s disease［J］. Cell Mol Life Sci, 2013, 70(3):459-473.

［24］Van Kampen JM, Robertson HA. A possible role for dopamine D 3, receptor stimulation in the induction of neurogenesis in the adult rat substantia nigra［J］. Neuroscience, 2005, 136(2):381-386.

［25］Crandall JE, Goodman T, Mccarthy DM, et al. Retinoic acid influences neuronal migration from the ganglionic eminence to the cerebral cortex［J］. J Neurochem, 2011, 119(4):723-735.

［26］Belinsky GS, Singh MB, Oikonomou KD, et al. Dopamine receptors in human embryonic stem cell differentiation［J］. Neuromethods, 2015, 96(10):229-249.

［27］Okeeffe GC, Barker RA, Caldwell MA. Dopaminergic modulation of neurogenesis in the subventricular zone of the adult brain ［J］. Cell Cycle, 2009, 8(18):2888-2894.

［28］Freundlieb N, Francois C, Tande D, et al. Dopaminergic substantia nigra neurons project topographically organized to the subventricular zone and stimulate precursor cell proliferation in aged primates［J］. J Neurosci, 2006, 26(8): 2321-2325.

［29］Takamura N, Nakagawa S, Masuda T, et al. The effect of dopamine on adult hippocampal neurogenesis［J］. Prog Neuropsychopharmacol Biol Psychiatry,2014, 50:116-124.

［30］Seidel JL, Faideau M, Aiba I, et al. Ciliary neurotrophic factor (CNTF) activation of astrocytes decreases spreading depolarization susceptibility and increases potassium clearance［J］. Glia, 2015, 63(1):91-103.

［31］Shimizu S, Tatara A, Sato M, et al. Role of cerebellar dopamine D3, receptors in modulating exploratory locomotion and cataleptogenicity in rats［J］. Prog Neuropsychopharmacol Biol Psychiatry, 2014, 50(2):157-162.

［32］Ikeda E, Matsunaga N, Kakimoto K, et al. Molecular mechanism regulating 24-hour rhythm of dopamine D3 receptor expression in mouse ventral striatum［J］. Mol Pharmacol, 2013, 83(5):959-967.

［33］Rangelbarajas C, Coronel I, Florán B. Dopamine receptors and neurodegeneration.［J］. Aging Dis, 2015, 6(5):349-368.

［34］Milosevic J, Schwarz SC, Maisel M, et al. Dopamine D2/D3 receptor stimulation fails to promote dopaminergic neurogenesis of murine and human midbrain-derived neural precursor cells in vitro［J］. Stem Cells Dev, 2007, 16(4):625-635.

［35］Madras BK. History of the discovery of the antipsychotic dopamine D2 receptor: a basis for the dopamine hypothesis of schizophrenia［J］. J Hist Neurosci, 2013, 22(1):62-78.

［36］Keilhoff G, Grecksch G, Bernstein HG, et al. Risperidone and haloperidol promote survival of stem cells in the rat hippocampus［J］. Eur Arch Psychiatry Clin Neurosci, 2010, 260(2):151-162.

［37］Wimalasena K. The inherent high vulnerability of dopaminergic neurons toward mitochondrial toxins may contribute to the etiology of Parkinson’s disease［J］. Neural Regen Res, 2016, 11(2):246-247.

［38］Blandini F, Armentero MT. Animal models of Parkinson’s disease［J］. FEBS J, 2012, 279(7):1156-1166.

［39］Park HJ, Shin JY, Lee BR, et al. Mesenchymal stem cells augment neurogenesis in the subventricular zone and enhance differentiation of neural precursor cells into dopaminergic neurons in the substantia nigra of a parkinsonian model.［J］. Cell Transplant, 2012, 21(8):1629-1640.

［40］Selvakumar GP, Janakiraman U, Essa MM, et al. Escin attenuates behavioral impairments, oxidative stress and inflammation in a chronic MPTP/probenecid mouse model of Parkinson’s disease［J］. Brain Res, 2014, 1585:23-36.

［41］Gal S, Zheng H, Fridkin M, et al. Restoration of nigrostriatal dopamine neurons in post-MPTP treatment by the novel multifunctional brain-permeable iron chelator-monoamine oxidase inhibitor drug, M30［J］. Neurotox Res, 2010, 17(1):15-27.

［42］Marxreiter F, Regensburger M, Winkler J. Adult neurogenesis in Parkinson’s disease［J］. Cell Mol Life Sci, 2013, 70(3):459-473.

［43］Peng J, Andersen JK. Mutant α-synuclein and aging reduce neurogenesis in the acute 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine model of Parkinson’s disease［J］. Aging Cell, 2011, 10(2):255-262.

［44］Ito T, Suzuki K, Uchida K, et al. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced neuroblastic apoptosis in the subventricular zone is caused by 1-methy-4-phenylpiridinium (MPP+) converted from MPTP through MAO-B［J］. Exp Toxicol Pathol, 2012, 64(7-8):761-765.

［45］Xi JH, Nakayama H. Transiently impaired neurogenesis in MPTP mouse model of Parkinson’s disease［J］. Neurotoxicology, 2015, 50:46-55.

［46］Schwerk A, Altschüler J, Roch M, et al. Human adipose-derived mesenchymal stromal cells increase endogenous neurogenesis in the rat subventricular zone acutely after6-hydroxydopamine lesioning［J］. Cytotherapy, 2015, 17(2):199-214.

［47］Cova L, Armentero MT, Zennaro E, et al. Multiple neurogenic and neurorescue effects of human mesenchymal stem cell after transplantation in an experimental model of Parkinson’s disease［J］. Brain Res, 2010, 1311(1):12-27.

［48］Matsui H, Gavinio R, Takahashi R. Medaka fish Parkinson’s disease model［J］. Exp Neurobiol, 2012, 21(3):94-100.

［49］Chen C, Chan A, Han W, et al. Stem and progenitor cell-derived therapies for neurological diseases［J］. Trends Mol Med, 2015, 21(11):715-729.

［50］Zhang P, Qi ShSh, Xie MQ, et al. Effect of allopregnanolone on the dopaminergic neurons in the substantia nigra of APPswe /PSEN1 mice ［J］. Acta Anatomica Sinica, 2015, 46(3):317-323 (in Chinese).

张鹏,戚双双,谢明琦,等. 别孕烯醇酮对APPswe/PSEN1小鼠黑质多巴胺能神经元的影响［J］.解剖学报,2015,46(3):317-323.

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神经增生在神经性毒物诱导的帕金森病动物模型中的研究进展

Current status of neurogenesis in neurotoxin-induced animal models for Parkinson’s disease

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