[1]Vicini S, Wang J F, Li J H, et al. Functional and pharmacological differences between recombinant N-methyl-D-aspartate receptors[J]. J Neurophysiol, 1998, 79(2): 555-566.[2]王晓鹏, 黄永杰, 王芳, 等. NMDAR、NR2A、NR2B与糖尿病认知功能障碍的关系[J]. 南方医科大学学报, 2013, 33(12): 1848-1851.[3]Madry Christian, Mesic Ivana, Bartholomäus Ingo, et al. Principal role of NR3subunits in NR1/NR3 excitatory glycine receptor function [J]. Biochem Biophys Res Commun, 2007, 354(1): 102-108.[4]陈松芳, 黄汉津, 王小同. NMDA受体NR1亚单位与学习记忆[J].中国行为医学科学, 2006, 15(1): 91. [5]Chung H J, Huang Y H, Lau L F, et al. Regulation of NMDA receptor complex and trafficking by activity-dependent phosphorylation of the NR2B subunit PDZ ligand [J]. J Neuroscience, 2004, 24(45): 10248-10259.[6]Bliss T V. Young receptors make smart mice [J]. Nature, 1999, 401(6748):25-27.[7]Goebel D J, Poosch M S. NMDA receptor subunit gene expression in the rat brain: a quantitative analysis of endogenous mRNA levels of NR1Com, NR2A, NR2B, NR2C, NR2D and NR3A [J]. Brain Res Mol Brain Res, 1999, 69(2): 164-170.[8]Kuriyama I, Asano N, Kato I, et al. Dipeptide alcohol-based inhibitors of eukaryotic DNA polymerase alpha [J]. Bioorg Med Chem, 2005, 13(6): 2187-2196.[9]杨宝峰. 药理学(第八版)[M]. 北京: 人民卫生出版社, 2013: 110-125.[10]楚世峰, 陈乃宏. 突触内外NMDA 受体的分布调控及其生物学功能[J]. 神经药理学报, 2011, 1(5): 40-48.[11]王传功, 徐霞, 库宝善. NMDA 受体与帕金森氏病[J]. 济宁医学院学报, 2000, 23(2) :75-76.[12] Abekawa Tomohiro, Ohmori Tetsuro, Ito Kouichi, et al. D1 dopamine receptor activation reduces extracellular glutamate and GABA concentrations in the medial prefrontal cortex[J]. Brain Res, 2000, 867(1-2): 250-254.[13]王爽, 高捷, 苏兴利, 等. 帕金森病模型大鼠内侧前额叶皮层锥体神经元NMDA受体敏感性下降[J].中国现代医学杂, 2014, 24 (1): 1-4.[14] Faucard Raphael, Armand Vincent, Heron Anne, et al. N-methyl-D-aspartate receptor antagonists enhance histamine neuron activity in rodent brain[J]. J Neurochem, 2006, 98(5):1487-1496.[15]Jones Susan, Alasdair J Gibb. Functional NR2B-and NR2D-containing NMDA receptor channels in rat substantia nigra dopaminergic neurones[J]. J Physiol, 2005, 569(Pt1): 209-221.[16]杨辉, 张可成, 蔡文琴. PD 鼠纹状体内NMDA受体密度及黑质内NMDA受体mRNA含量的观察[J]. 第三军医大报, 1996, 18(3): 206-208.[17] Armentero Marie-Therese, Fancellu Roberto, Nappi Giuseppe, et al. Prolonged blockade of NMDA or mGluR5 glutamate receptors reduces nigrostriatal degeneration while inducing selective metabolic changes in the basal ganglia circuitry in a rodent model of Parkinson’s disease[J]. Neurobiol Dis, 2006, 22(1): 1-9.[18]Turle-Lorenzo Nathalie, Breysse Nathalie, Baunez Christelle, et al. Functional interaction Between mGlu5 and NMDA receptors in a rat model of Parkinson’s disease[J]. Psychopharmacology(Berl), 2005, 179(1): 117 -127.[19]王传功, 王旭, 齐汝霞. NMDA和GABA受体拮抗剂对帕金森模型小鼠神经细胞的影响[J]. 济宁医学院学报, 2006, 29(2):20-21. [20]王传功, 徐霞, 库宝善. NMDA受体和GABA受体拮抗剂对小鼠帕金森模型的行为药理学影响[J].中国行为医学科学, 1998, 7(1): 19-21.[21]王传功, 徐霞, 辛勤, 等. NMDA 受体拮抗剂和GABA 受体拮抗剂对小鼠帕金森模型的影响[J]. 济宁医学院学报, 1998, 21(3): 8-10. [22]Steece-Collier K, Chambers L K, Jaw-Tsai S S, et al. Antiparkinsonian actions of CP101, 606, an antagonist of NR2B subunit-containing N-methyl-D-aspartate receptors [J]. Exp Neurol, 2000, 163(1):239-243.[23]张奇. 铅暴露AD模型大鼠脑不同区域NMDA受体亚基(NR1、NR2A、NR2B)表达的研究[D]. 江苏:中国药科大学, 2007, 1-20.[24]Behe P, Stern PWyllie D J, Nassar M, et al. Determination of NMDA NR1 subunit copy number in recombinant NMDA receptors[J]. Proc Biol Sci, 1995, 262(1364): 205-213.[25]Mony Laetitia, Kew James N C, Martin J Gunthorpe, et al. Allosteric modulators of NR2B-containing NMDA receptors: molecular mechanisms and therapeutic potential[J]. Br J Pharmacol, 2009, 157(8): 1301-1317.[26] Bi Hong, Sze Chun-I. N-methyl-d-aspartate receptor subunit NR2A and NR2B messenger RNA levels are altered in the hippocampus and entorhinal cortex in Alzheimer' s disease[J]. Neurological Sciences, 2002, 200(1-2):11-18[27]刘志安, 赵娓娓, 吕春娥, 等. AD样大鼠海马NMDAR亚单位2B和2A的表达及其与细胞凋亡的关系[J]. 山东大学学报(医学版), 2011, 49(2): 14-18.[28] Shirley W Y Tsanq, Harry V Vinters, Jeffrey L Cumminqs, et al. Alterations in NMDA receptor subunit densities and ligand binding to glycine recognition sites are associated with chronic anxiety in Alzheimer’s disease[J]. Neurobiol Aging, 2008, 29(10): 1524-1532.[29]吴婷, 丁新生, 董海蓉, 等. NMDA受体拮抗剂对Aβ42基因果蝇阿尔茨海默病模型的神经保护作用[C]. 全国抗衰老与老年痴呆学术会议论文汇编, 2009: 37.[30]曹续政, 张黎明, 沈月娥, 等. NMDA受体介导了加兰他敏对阿尔茨海默病大鼠认知功能的改善[J]. 中风与神经疾病杂志, 2006, 23(6): 678-680.[31]李玺, 袁海峰, 张智燕. 脑尔康对AD 模型小鼠脑内NMDA受体亚单位NR2B表达的影响[J]. 中国医药学报, 2004, 19(1): 11-14.[32]李玺, 刘颖, 张欣, 等. 人参皂苷Rg1对大鼠脑片AD模型磷酸化Tau蛋白及NMDA受体亚单位NR1, NR2B表达的影响[J]. 中国中药杂志, 2010, 35(24): 3339-3343.[33] Alice Wexler. Stigma, history, and Huntington' s disease[J].Lancet, 2010, 376(9734): 18-19.[34]沈原.亨廷顿病发病机制的研究进展[J].国际神经病学神经外科学杂志, 2010, 37(1) : 70-72.[35]Warby S C, Montpetit AHayden A R, Carrol J B, et al. CAG expansion in the Huntington disease gene is associated with a specific and targetable predisposing haplogroup[J].Am J Hum Genet, 2009, 84(3): 351-366.[36]袁维秀, 杨红菊. N-甲基-D-天冬氨酸-2B 受体功能的研究进展[J]. 国外医学药学分册, 2004, 31(3): 146-149.[37]Hodgson J Graeme, Agopyan Nadia, Gutekunst Claire-Anne, et al. A YAC mouse model for Huntington’s disease with full-length mutant huntingtin, cytop lasmic toxicity, and selective striatal neurodegeneration[J]. Neuron, 1999, 23(1):181-192.[38]Sammels Eva, Parys Jan B, Missiaen Luding, et al.Intracellular Ca2+ storage in health and disease: A dynamic equilibrium[J]. Cell Calcium, 2010, 47(4): 297-314.[39]Lau A, Tymianski M. Excitotoxicity [M]. Oxford: Pergamon Press, 2010: 515-535.[40] Shehadeh Jacqueline, Fernandes Herman B, Zeron Mullins Melinda M, et al. Striatal neuronal apoptosis is preferentially enhanced by NMDA receptor activation in YAC transgenic mouse model of Huntington disease[J]. Neurobiol Dis,2006,21(2) : 392-403.[41]Olney J W. New insights and new issues in developmental neuro toxicology[J]. Neurotoxicology, 2002, 23(6):659-668.[42] Verhagen M L, Morris M J, Farmer C, et al.Huntington's disease: A randomized,controlled trial using the NMDA antagonist amantadine [J]. Neurology, 2002, 59 (5): 694-699.[43]Mary V, Wahl F, Stutzmann J M. Effect of riluzole on quinolinate-induced neuronal damage in rats: comparison with blockers of glutamatergic neurotransmission [J]. Neurosci Lett, 1995, 201(1): 92-96.[44]Schiefer Johannes, Landwehrmeyer G Bernhard, Lüesse Hans-Gerd, et al.Riluzole prolongs survival time and alters nuclear inclusion formation in a transgenic mouse model of Huntington' s disease[J].Mov Disord, 2002, 17(4): 748-757.[45]Seppi Klaus, Mueller Joerg, Bodner Thomas, et al. Riluzole in Huntington's disease (HD): an open label study with one year follow up [J]. J Neurol, 2001, 248(10):866-869.[46]李晓光, 崔丽英. 肌萎缩侧索硬化的现代治疗[J]. 中国现代医药杂志, 2013,15(11): 97-101.[47] Zhi Qi-xiong, McNamara James O. Fas(t) balls and Lou Gehrig disease. A clue to selective vulnerability of motor neurons? [J]. Neuron, 2002, 35(6):1011-1013.[48] von Lewinski Friederike, Keller BernhardU. Ca2 +, mitochondria and selective motoneuron vulnerability: implications for ALS [J]. Trends Neurosci, 2005, 28(9):494 -500.[49]郑梅, 樊东升. NMDA受体不同亚单位分布造成肌萎缩侧索硬化中运动神经元选择性易损[J]. 北京大学学报(医学版), 2011, 43(2): 228-233.[50]Miller R G, Mitchell J D, Lyon M.Riluzole for amyotrophic lateral sclerosis ( ALS ) / motor neuron disease ( MND )[J].Cochrane Database Syst Rev,2012, 3: CD0 01447.[51]Lee C T, Chiu Y W, Wang K C, et al.Riluzole and prognostic factors in amyotrophic lateral sclerosis long-term and short-term survival: a population-based study of 1149 cases in Taiwan[J]. J Epidemiol, 2013, 23(1): 35-40. |