期刊文献+

NMDA受体NR2A,NR2B亚基对大鼠脑缺血再灌注海马CA1区神经细胞损伤的作用 被引量:2

Effect of NMDA receptor subunits NR2A and NR2B on transient brain ischemia/reperfusion-induced neuronal death in rat hippocampus
原文传递
导出
摘要 目的观察N-甲基-D-天冬氨酸受体(NMDA)NR2A,NR2B亚基对脑缺血-再灌注后海马CA1区神经细胞存活的不同影响。方法采用Pulsinelli-Brierley四动脉阻塞(4-VO)大鼠全脑缺血模型,缺血前连续3天脑室注射NR2A,NR2B反义寡核苷酸(ASODN)后缺血15min,复灌5d,石蜡切片,以焦油紫染色,图像分析测定单位面积内焦油紫染色细胞面积总和,与缺血组及错义寡核苷酸组(MSODN)进行形态学分析。结果NR2A、NR2B反义寡核苷酸对脑缺血再灌注后海马CA1神经细胞均有明显保护作用,以NR2A AS ODN保护作用更明显,与缺血组比较约有50%细胞存活(P<0.05)。结论NR2A,NR2B亚基的含量降低对脑缺血再灌注后海马神经细胞有明显保护作用。 Objective To investigate the role of NR2A, NR2B [the subunits of N-methyl-Dasparate(NMDA) receptor] on the neuronal death induced by transient cerebral ischemia. Methods Transient (15 rain) brain ischemia was induced by the four-vessel occlusion in Sprague Dawley rats. The antisense oligodeoxynucleotides (ODNs) of NR2A and NR2B were used to suppress the expression of NR2A and NR2B by intracerebroventricular intracerebroventricular infusion once per day for 3 days before ischemia. After 5 days reperfusion, the rats were perfusion -fixed with paraformaldehyde and cresyl violet staining was used to examine the survival of CA1 pyramidal cells of the hippocampus. Results Both NR2A and NR2B antisense ODNs showed a protective effect against neuronal cell death induced by cerebral ischemia/reperfusion. Furthermore, NR2A antisense ODNs had more protective effect on the neuronal death than NR2B antisense ODNs (P〈0. 05). Conclusion Both NR2A and NR2B suhunits play an important role in neuronal death induced by cerebral ischemia followed by reperfusion.
出处 《江苏医药》 CAS CSCD 北大核心 2009年第1期81-83,I0004,共4页 Jiangsu Medical Journal
基金 江苏省自然科学基金(BK2006536) 国家自然科学基金(30800309)
关键词 N-甲基-D-天冬氨酸受体 NR2A NR2B 反义寡核苷酸 脑缺血 海马 N-methyl-D-asparate (NMDA) receptor NR2A NR2B Antisense oligodeoxynucleotides (ODNs) Cerebral ischemia Hippocampus
  • 相关文献

参考文献10

  • 1Pei DS, Wang XT, Liu Y, et al. Neuroprotection against ischaemic brain injury by a GluR6-gc peptide containing the TAT protein transduction sequence [J]. Brain, 2006, 129 (2) : 465-479.
  • 2Hattori H, Wasterlain CG. Excitatory amino acids in the developing brain: ontogeny, plasticity, and excitotoxicity [J]. Pediatr Neurol, 1990,6(4): 219-228.
  • 3Wang C, Fridley J, Johnson KM. The role of NMDA receptor upregulation in phencyclidine-induced cortical apoptosis in organotypic culture [ J ]. Biochem Pharmacol, 2005, 69 ( 9 ) : 1373-1383.
  • 4Pulsinelli WA, Brierlsy JB. A new model of bilateral hemispheric ischemia in the unanesthetized rat[J]. Stroke, 1979, 10(3):267-272.
  • 5Choi DW. Calcium: still center-stage in hypoxic-ischemic neuronaldeath[J]. J Trend Neurosci, 1995,18 (2) : 58-60.
  • 6Hollnann M, Heinemann S. Cloned glutamate receptor[J]. Ann Rev Neurosci, 1994, 17(3) :31-108.
  • 7Wenthold RJ, Prybylowski K, Standley S, et al. Trafficking of NMDA receptors [J].Annu Rev Pharmacol Toxicol, 2003,43:335-358.
  • 8Qian Chen, Songtao He, Xiao-Ling Hu, et al. Differential roles of NR2A- and NR2B-containing NMDA receptors in activity-dependent brain-derived neurotrophic factor gene regulation and limbie epileptogenesis[J]. Neuroscience, 2007, 27(3):542-555.
  • 9Besshoh S, Bawa D, Teves L, et al. Increased phosphorylation and redistribution of NMDA receptors between synaptic lipid rafts and post-synaptic densities following transient global ischemia in the rat brain[J]. J Neurochem, 2005, 93 (1):186-194.
  • 10Liu Y, Hou XY, Zhang GY, et al. L-type voltage-gated calcium channel attends regulation of tyrosine phosphorylation of NMDA receptor subunit 2A induced by transient brain ischemia [J]. Brain Res,2003,972(1-2):142-148.

同被引文献54

  • 1刘旭.细胞粘附分子引起脑缺血再灌注损伤机制的研究[J].中外健康文摘:临床医师,2008,0(3):1-3. 被引量:1
  • 2刘宝松,陈恒胜,许忠,陈力学,曾琳,龙在云.缺氧所致神经元AMPA受体的结构组成及功能变化[J].第三军医大学学报,2004,26(23):2139-2142. 被引量:5
  • 3张隽,丰宏林,姜海智,盛莉,孙威.N-甲基-D-天门冬氨酸受体-1反义寡核苷酸对大鼠脑缺血性损伤的保护作用[J].中国脑血管病杂志,2006,3(5):228-231. 被引量:2
  • 4Roberts-Lewis JM, Savage MJ, Marcy VR, et al. Immunolocalization of calpain I-mediated spectrin degradation to vul- nerable neurons in the ischemic gerbil brain[J] J Neurosci. 1994, 14 (06): 3934-3944.
  • 5Weber JT, Rzigalinski BA, Willoughby KA, et al. Alterations in calcium-mediated signal transduction after traumatic injury of cortical neurons [J]. Cell Calcium, 1999, 26 (06): 289-299.
  • 6Niwa M, Inao S, Takayasu M, et al. Time course of expression of three nitric oxide synthase isoforms after transient middle cerebral artery occlusion in rats [J]. Neurol Med Chir (Tokyo), 2001, 41 (02) : 63-73.
  • 7Muramatsu K, Sheldon RA, Black SM, et al. Nitric oxid synthase activity and inhibition after neonatal hypoxia isehe- mia in the mouse brain [J]. Brain Res Dev Brain Res, 2000, 123 (02): 119-127.
  • 8Huang, PL. Neuronal and endothelial nitric oxide synthase gene knockout mice [J]. Braz J Med Biol Res, 1999, 32 (11): 1353-1359.
  • 9Xu J, He L, Ahmed SH, et al. Oxygen-glucose deprivation induces inducible nitric oxide synthase and nitrityrosine ex- pression in cerebral endotheial cell [J]. Stroke, 2000, 31 (07) : 1744-1745.
  • 10Iadecola C, Niwa K, Nogawa S, et al. Reduced susceptibility to ischemic brain injury and N-methyl-D-aspartate-media- ted neurotoxicity in cyclooxygenase-2-deficient mice [J]. Proc Natl Acad Sci USA, 2001, 98 (03) : 1294-1299.

引证文献2

二级引证文献6

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部