期刊文献+

惊厥大鼠不同脑区突触体内单胺类递质水平的动态变化及意义

Dynamic Changes and Significence of Synaptic Monoamine Transmitter Levels in Different Brain Regions of Epileptic Rats
下载PDF
导出
摘要 目的探讨单胺类递质与惊厥的关系。方法选用Wistar大鼠32只,采用腹腔注射硫代氨基脲制作惊厥模型。取大脑皮层、海马、纹状体三个脑区,制备出突触小体。用荧光分光光度计测定五羟色胺(5-HT)、多巴胺(DA)、去甲肾上腺素(NA)三种单胺类递质的含量。结果 5-HT含量在惊厥发作组中,大脑皮层和海马区显著下降(P<0.01),而纹状体仅致死组有明显降低(P<0.01);DA含量在惊厥组中仅纹状体有显著下降(P<0.01);而大脑皮层和海马区无明显变化(P>0.05);NA含量在惊厥组中,仅海马区有明显下降(P<0.01);而大脑皮层则随惊厥初发、再发和致死组反见升高;在纹状体,致死组有明显下降(P<0.05)。结论惊厥的发生、发展与特定脑区突触体内特定的单胺类递质含量有关,并非所有脑区突触体内出现普遍性单胺类递质的下降;不同部位的神经递质与惊厥的敏感性和发作严重程度有关。 Objective To explore the relation between monoamines and epilepsy.Methods The rat model of seizure was made by intraperitoneal injection.The palium(Pal),hippocampus(Hip)and corpus striatum(Str) were taken immediately and the brain synaptosomes were prepared after the rats were sacrificed.The levels of serotonin(5-HT),dopamine(DA) and norepinephrine(NA)in synaptosomes were determined by fluorescence spectrophotometer.Results The levels of 5-HT decreased significantly in Pal and Hipin from experimental groups(P〈0.01),but decreased in Str from lethal group(P〈0.01).The levels of DA decreased significantly only in Str from convulsive groups(P〈0.01).The levels of NA markedly decreased only in Hip from convulsive groups(P〈0.01),While in Pal,it increased with the consequence of incipience,relapse and death.In Str,DA levels decreased markedly only in lethal grop(P〈0.05).Conclusion The onset and development of epilepsy are related to the levels of certain monoamine in synaptosomes of cerain brain regions.The transmitters in different regions may affect the sensitivity and be related to the severity of epilepsy.
出处 《南昌大学学报(医学版)》 CAS 2010年第5期13-15,共3页 Journal of Nanchang University:Medical Sciences
关键词 惊厥 大脑皮质 海马 纹状体 单胺类神经递质 突触小体 动物 实验 大鼠 epilepsy palium hippocampus striatum monoamine synaptosome animals laboratory rats
  • 相关文献

参考文献3

二级参考文献49

  • 1Lynch M, Sutula T. Recurrent excitatory connectivity in the dentate gyrus of kindled and kainic acid-treated rats[J]. J Neurophysiol, 2000,83 (2) : 693- 704.
  • 2Blair RC, Sombati S, Lawrence DC, et al. Epileptogenesis causes acute and chronic increases in GABA(A) receptor endocytosis that contributes to the induction and maintenance of seizures in the hippocampal culture model of acquired epilepsy[J]. J Pharmacol Exp Ther. 2004,310: 871-879.
  • 3Furtinger S, Bettler B, Sperk G. Altered expression of GABAB receptor in the hippocampus after kainic-acid-induced srizures in rats[J]. Mol Brain Res, 2003,113:107-115.
  • 4Tdfeian AE, Tseng HC, Baybis M, et al. Differential expression of GABA and glutamate-receptor subunits and enzymes involved in GABA metabolism between electrophysioiogically identified hippocampal CA1 pyramidal cells and interneurons[J]. Epilepsia, 2003,44 (2) : 143-149.
  • 5Bernard C, Cossart R, Hirsch JC, et al. What is GABAergic inhibition? How is it nodified in epilepsy? [J] Epilepsia, 2000,41 (suppl 6 ) : 890-895.
  • 6Burazin TC, Gundlach AL. Rapid but transient increases in choleeystokinin mRNA levels in cerebral cortex following amygdaloid-kindled seizures in the rat[J]. Neurosci Lett, 1996,209(1) :65-68.
  • 7Cobbi M, Menini T, Vezzani A, et al. Autoradiographic reevaluation of the binding properties of ^125Ⅰ-[Leu31,Pro34]peptide YY and ^125Ⅰ-peptide YY3-36 to neuropeptide Y receptor subtypes in rat forebrain[J]. J Neurochem, 1999,72(4) : 1663-1670.
  • 8Kofler N, Kirchmair E, Sehwarzer C, et al. Altered expression of NPY- Y1 receptors in kainic acid induced epilepsy in rats[J]. Neurosci Lett, 1997,230 (2): 129-132.
  • 9Schwarzer G, Kofler N, Sperk G. Up-regulation of neuropeptide Y-Y2 receptors in an animal model of temporal lobe epilepsy[J]. Mol Pharmacol, 1998,53(1) :6-13.
  • 10Parker RM, Herzon H. Gomparison of Y-receptor subtype expression in the rat hippocampus[J]. Regul Pept,1998,75-76(25) :109-115.

共引文献23

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