期刊文献+

GAD67/GAD65在颞叶癫痫大鼠海马内源性促痫机制中的作用

The ratio of GAD67/GAD65 in self-acceleration mechanisms in the hippocampus of temporal lobe epilepsy rats
原文传递
导出
摘要 目的 探讨GAD6 7/GAD6 5在颞叶癫痫发生后大鼠海马内源性促痫机制中的作用。方法  112只雄性SD大鼠随机分为实验组 (n =70 )与对照组 (n =4 2 ) ,实验组大鼠选用海人酸腹腔注射法建立颞叶癫痫模型 ,对照组大鼠腹腔注射无菌生理盐水。选取腹腔注射后 3h、6h、12h、2 4h、4 8h、7d、30d为研究的时间点 ,颞叶海马的CA1区、CA3区、齿状回为研究部位。腹腔给药后每天观察大鼠的行为学变化 ,大鼠处死前进行EEG描记。免疫组织化学法检测GAD6 5、GAD6 7蛋白的表达。结果 海人酸致痫后 6h ,实验组大鼠海马CA1区、CA3区GAD6 7/GAD6 5的比率较对照组升高 (P <0 .0 1) ;海人酸致痫后 30d ,实验组大鼠海马齿状回GAD6 7/GAD6 5的比率较对照组降低 (P <0 .0 5 )。结论 颞叶癫痫急性期CA1区、CA3区GAD6 7/GAD6 5比率的增高及慢性期齿状回GAD6 7/GAD6 Objective To discuss the effect of GAD67/GAD65 on endogenous self acceleration mechanism in hippocampus after seizures.Methods Epileptic rats were injected with kainate intraperitoneally to establish temporal lobe epilepsy model,and the controls were injected with saline instead of kainate. At 3 h,6 h,12 h,24 h,48 h and 7 d, 30 d after kainate injection, the rats in two groups were anaesthetized and perfused and EEGs were recorded antemortem.By use of immunohistochemistry, the GAD65 and GAD67 protein was analyzed at different time quantitatively in the dentate gyrus,CA1 and CA3 regions of hippocampus.Results The GAD67/GAD65 ratio increased at 6 h in CA1 and CA3 regions following the onset of seizure and decreased at 30 days in dentate gryus.Conclusions The up regulation of GAD67/GAD65 ratio in CA1 and CA3 regions in acute temporal lobe epilepsy and the low regulation of GAD67/GAD65 ratio in dentate gryus of chronic temporal lobe epilepsy could be the important factors in the occurrence of epilepsy and the self protection mechanism after seizures.
出处 《卒中与神经疾病》 2004年第5期279-282,共4页 Stroke and Nervous Diseases
关键词 GAD 大鼠海马 对照组 海人酸 CA3区 齿状回 癫痫 雄性 CA1区 行为学 Kainite Temporal lobe epilepsy GAD65 GAD67 Self-acceleration
  • 相关文献

参考文献11

  • 1Battaglioli G, Liu H, Martin DL. Kinetic differences between the isoforms of glutamate decarboxylase: implications for the regulation of GABA synthesis. J Neurochem, 2003,86 (4): 879-887.
  • 2Telfeian AE, Tseng HC, Baybis M, et al. Differential expression of GABA and glutamate-receptor subunits and enzymes involved in GABA metabolism between electrophysiologically identified hippocampal CA1 pyramidal cells and interneurons. Epilepsia, 2003,44 (2): 143-149.
  • 3Curran-Rauhut MA, Petersen SL. Regulation of glutamic acid decarboxylase 65 and 67 gene expression by ovarian steroids:identification of two functionally distinct populations of GABA neurones in the preoptic area. J Neuroendocrinol,2002,14(4) :310-317.
  • 4黄理金.大鼠海人酸致痫模型的症状表现、致痫机制的研究进展[J].国外医学(神经病学.神经外科学分册),2001,28(5):339-342. 被引量:9
  • 5Wong CG, Bottiglieri T, Snead OC 3rd. GABA, gamma-hydroxybutyric acid and neurological disease. Ann Neurol, 2003,54 (Suppl 6):S3-12.
  • 6Mason GF, Martin DL, Martin SB, et al. Decrease in GABA synthesis rate in rat cortex following GABA-transaminase inhibition correlates with the decrease in GAD(67) protein. Brain Res, 2001,914(1-2):81-91
  • 7Dkhissi O, J ulien J F, Wasowicz M, et al. Differential expression of GAD(65) and GAD(67) during the development of the rat retina.Brain Res, 2001,919 (2): 242-249.
  • 8Pompolo S, Scott CJ, Clarke IJ. Selective regulation of glutamic decarboxylase isoform 65, but not isoform 67, in the bed nucleus of the stria terminalis and the preoptic area of the ewe brain across the estrous cycle. Endocrinology,2002,143(2) :544-550.
  • 9Esclapez M, Hoser CR. Up-regulation of GAD65 and GAD67 in remaining hippocampal GABA neurons in a model of temporal lobe epilepsy. J Comp Neurol, 1999,412(3) :488-505.
  • 10Rougeulle C, Lalande M. Angelman syndrome: how many genes to remain silent? Neurogenetics, 1998,1 (4): 229-237.

二级参考文献19

  • 1Ben- Ari Y. Limbic seizure and brain damage Poduced by kainic acid:mechanisms and relevance to human temporal lobe epilepay.Neuroscience. 1985; 14(2) :375 - 405
  • 2Wilson CL, Maidment NT, Shomer MH, et al. Comprison of seizure related amino acid release in human eplepic hippocampas versus a chronic, kainite rat model of hippocampal epilepsy. Epilepsy Res, 1996,26(1):245-254
  • 3Simntov R, Crispino M, Hoe W, et al. Changes in expression of neuronal and glial glutamate transporters in rat hippocampus following kainite - induced seizure activity. Brain Res Mol Brain Res, 1999,65( 1 ): 112 - 123
  • 4Rafiki A, Ben - Ari Y, khrestchatisky M et al. Long - lasting enhanced expression in epilepsy. Eur J Neurosci, 1998,10(2) :497 - 507
  • 5Babb TL, Mathem GW, Leite JP et al. Glutamate AMP receptors in the fascia dentate of human and kainite rat hippocampal epilepsy. Epilepsy Res. 1996,26(1):193 - 205
  • 6Blumcke I, Becker A J, Klein C, et al. Temporal lobe epilepsy associated up- regulation of metabotropic glutamate receptors: Correlatd Changes in MgluR1 mRNA and rotein expression in exPerimental animals and human Ptients. J Neuropathol Exp Neurol.2000,59(1): 1 - 10
  • 7White HS. Comparative anticonvulsant and mechanistic profile of the established and newer antiepileptic drugs. Epilepsia, 1999.40 Suppl 5:S2- 10
  • 8Loscher W, Lehmann H, Behl B, et al. A new Prrolyl - quinoxalinedione series of non - NMDA glutamate receptor antagonists: Parmacological characterization and comparison with NBQX and valproate in the lindling model of epilepsy. Eur J Neurosci, 1999,11 ( 1 ) :250 - 262
  • 9Rodriguez MA, Herreras O, Lerma J, et al. Kainate receptors tresynaptically downregulate GABA ergic inhibition in the rat hippocampus. Neuron. 1997,19(4): 893 - 901
  • 10Friedman LK, Pllegrini- GiamPetro DE, Seperber EF, et al. kainate -induced status epilepticus alters glutamate and GABA receptor gene expression in adult rat hippocampus: an in situ hybridization study. J Neurosci, 1994,14(5Pt1 ): 2697 - 2707

共引文献8

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