期刊文献+

代谢型谷氨酸受体在癫幼鼠模型海马组织中的表达

Expression of Metabolic Pattern Glutamic Acid Receptor in Hippocampus of Juvenile Rat Model of Epilepsy
原文传递
导出
摘要 目的探讨癫模型幼鼠海马组织中代谢型谷氨酸受体R1及R3(mGluR1和mGluR3)的表达变化及其作用机制。方法给予幼鼠腹腔注射氯化锂-匹罗卡品,观察幼鼠的行为变化,把发作程度达到Racine 5级并持续6 h以上的动物认为匹罗卡品癫持续状态动物模型制作成功,归入实验组,未达到该标准或抽搐致死的幼鼠剔除。实验SD幼鼠共18只,随机分为下列各组(每组6只):癫发作后6 h组(急性期,Ⅰ组),5 d组(静止期,Ⅱ组)及60 d组(慢性期,Ⅲ组)。9 g/L盐水腹腔注射18只(对照组),每组6只,与实验组的时间点相对应,分为6 h组(Ⅰa组),5 d组(Ⅱa组)及60 d组(Ⅲa组)。分别在各时间点处死动物取脑海马组织,处死动物前行常规脑电图(EEG)检查。应用反转录聚合酶链反应(RT-PCR)方法检测各组脑海马组织中mGluR1和mGluR3表达。结果Ⅰ组幼鼠EEG均异常;Ⅱ组幼鼠EEG正常;Ⅲ组5只幼鼠(83%)出现散发尖波、棘波或棘慢波。对照组未出现自发发作。分别与Ⅰa组、Ⅱa组比较,Ⅰ组及Ⅱ组幼鼠mGluR1 mRNA表达水平显著上调,差异有显著性(Pa<0.01);Ⅲ组mGluR1 mRNA表达水平与Ⅲa组相比,无显著性差异(P>0.05)。与相应的Ⅰa、Ⅱa、Ⅲa组比较,Ⅰ、Ⅱ、Ⅲ组的mGluR3 mRNA表达水平均上调,有显著性差异(Pa<0.01)。结论mGluR1表达上调可能促进了兴奋性毒作用,而晚期mGluR3表达上调可能有利于海马组织的保护作用。 Objective To investigate the changes and possible mechanisms of the expressions of metabolic pattern glutamic acid receptor 1(mGluR1) and mGluR3 in hippocampus of juvenile rats submitted to lithium chloride - pilocarpine induced model of epilepsy in 6 h,5 d, 60 d after status epilepticus(SE) onset. Methods Seizures were induced in the juvenile rats with lithium and pilocarpine injected intraperitoneally, and behavioral changes and EEG were observed. Eighteen SD juvenile rats with SE were randomly divided into following groups : group Ⅰ ,in which the rats were killed at 6 h after SE onset (6 h SE), group Ⅱ ,in which the animals were killed during the seizure - free period (5 days after SE onset), and group m ,in which the animals were killed in 60 days after SE induction (period of spontaneous recurrent seizures). And intraperitoneal injection of saline water control groups were divided into: group Ⅰa, group Ⅱa and group Ⅲ a. The hippocampus tissues after the rats were put to death were collected, the expressions of mGluR1 and mGluR3 mRNA were detected by reverse transcriptase polymerase chain reaction ( RT - PCR) in the hippocampus of juvenile rats. Results EEG of rats in group Ⅰ were abnormal, but normal in group Ⅱ , and 5 ( 83 % ) cases of the juvenile rats in group Ⅲ manifested dissemination of sharp waves, spikes or spike wave. The saline control group did not spontaneously attack. There was more significant upregulation of mGluR1 mRNA expression ( Pa 〈 0.01 ) in group [ and the group Ⅱ, and there was no alteration in group Ⅲ( P 〉 0.05 ). The expressional levels of mGluR3 mRNA were upregulated in group Ⅰ , group Ⅱ and group Ⅲ (Pa 〈0.01 ). Conclusion An altered balance between the mGluR1 and mGluR3 may play an important roles in the onset and maintenance of epilepsy.
出处 《实用儿科临床杂志》 CAS CSCD 北大核心 2009年第18期1442-1443,1456,共3页 Journal of Applied Clinical Pediatrics
基金 河南省教育厅项目资助(2008A320053)
关键词 代谢型谷氨酸受体 癫痫模型 氯化锂-匹罗卡品 癫痫持续状态 metabolic pattern glutamic acid receptor epilepsy model lithium chloride - pilocarpine status epilepticus
  • 相关文献

参考文献11

  • 1王琳,伍国锋,薛红,桑文华,仲伟斌.氯化锂毛果芸香碱癫癎鼠模型B_1与B_2激肽受体表达研究[J].中华老年心脑血管病杂志,2007,9(9):634-636. 被引量:4
  • 2李丹,黄绍平,张婕.氯化锂-匹鲁卡品诱发癫持续状态后大鼠脑组织主要穹隆蛋白的表达[J].实用儿科临床杂志,2008,23(12):952-954. 被引量:3
  • 3Bregola G, Varani K, Beani C, et al. Changes in hippocampal and cortical B1 bradykinin receptor biological activity in two experimental models of epilepsy [ J ]. Neuroscience, 1999,92 (3) : 1043 - 1 049.
  • 4Pereira MG, Gitai DL, Paco ML, et al. Modulation of B1 and B2 kinin receptors expression levels in the hippocampus of rats after andiogenic kindling and with limbic recruitment, a model of temporal lobe epilepsy [ J]. Immunopharmacol,2008,8 ( 2 ) :200 - 205.
  • 5Martin ED, Araque A, Buno W. Synaptic regulation of the slow Ca^2 + activated K^ + current in hippocampal CA1 pyramidal neurons: Implication in epileptogenesis [ J ]. J Neurophysiol, 2001,86 ( 6 ) : 2878 - 2888.
  • 6Siva JA, Goto EM, Perosa SR, et al. Kinin B1 receptors facilitate the development of temporal lobe epilepsy in mice [ J ]. Immunopharmacol, 2008,8(2) : 197 - 199.
  • 7梁承玮,杨伟力,邓欣.婴幼儿癫持续状态的现状与建议[J].实用儿科临床杂志,2008,23(12):968-972. 被引量:9
  • 8Karr L, Rutecki PA. Activity -dependent induction and maintenance of epileptiform activity produced by group I metabotropic glutamate receptors in the rat hippocampal slice[ J]. Epilepsy Res,2008,81 ( 1 ) : 14 - 23.
  • 9Meurs A, Clinckers R, Ebinger G. Seizure activity and changes in hippocampal extracellular glutamate, GABA, dopamine and serotonin[ J]. Epilepsy Res,2008,78( 1 ) :50 -59.
  • 10Imre G. The preclinical properties of a novel group II metabotropic glutamate receptor agonist LY379268 [ J ]. CArS Drug Rev, 2007,13 (4) : 444 - 464.

二级参考文献68

  • 1胡越,蒋莉.控制氯化锂-匹罗卡品诱发惊厥持续状态发作的实验研究[J].儿科药学杂志,2003,9(4):5-8. 被引量:25
  • 2张亮,徐杰丰,段德义.多药耐受基因家族与难治性癫痫[J].解剖科学进展,2006,12(1):72-74. 被引量:2
  • 3王凌霄,苗玲.难治性癫痫的耐药机制[J].上海交通大学学报(医学版),2006,26(11):1306-1309. 被引量:3
  • 4薛国芳,郑辑英,李光来,王荔,刘勇.氯化锂-匹罗卡品诱发大鼠癫痫持续状态后脑内c-fos蛋白表达的动态观察[J].中西医结合心脑血管病杂志,2007,5(5):419-420. 被引量:4
  • 5Racine RJ.Modification of seizure activity by electrical stimulation:Ⅱ.Motor seizure[J].Electroencephalogr.Clin Neurophysiol,1972,32:281-294.
  • 6Arganraz GA,Silva Jr JA,Perosa SR,et al.The synthesis and distribution of the kinin B1 and B2 receptors are modified in the hippocampus of rats submitted to pilocarpine model of epilepsy[J].Brain Res,2004,1006:114-125.
  • 7Volk HA,Arabadzisz D,Fritschy JM,et al.Antiepileptic drug-resistant rats differ from drug-responsive rats in hippocampal neurodegeneration and GABA receptor ligand binding in a model of temporal lobe epilepsy[J].Neurobiol Dis,2006,21:633-646.
  • 8Adolfo AG,Regina PS,Cristina LE,et al.Role of kinin B1 and B2 receptors in the development of pilocarpine model of epilepsy[J].Brain Res,2004,1013:30-39.
  • 9Felipe SA,Rodrigues ES,Marein RP,et al.Functional expression of kinin B1 and B2 receptors in mouse abdominal aorta[J].J Med Biol Res,2007,40:649-655.
  • 10Bregola G,Varani K,Beani C,et al.Changes in hippocampal and cortical B1 bradykinin receptor biological activity in two experimental models of epilepsy[J].Neuroscience,1999,92:1043-1049.

共引文献13

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