期刊文献+

调心方对β-淀粉样蛋白和皮质酮抑制大鼠海马脑片CA1区LTP的作用研究 被引量:3

Effects of Tiao-Xin-Fang on Long-term Potentiation Inhibited by β-amyloid and Corticosterone in Rat Hippocampal Slices
暂未订购
导出
摘要 采用细胞外微电极记录技术 ,观察调心方对 β 淀粉样蛋白和皮质酮抑制大鼠海马脑片LTP作用的影响。结果发现 ,在正常情况下 ,海马脑片LTP诱发成功率约为 6 0 % ,施以高频串刺激后PS幅度显著增高 ,PS潜伏期明显缩短。预先用 β 淀粉样蛋白 (0 2 μΜ )或皮质酮 (2 μM)孵育海马脑片对正常PS的形状、幅度无明显影响 ;但两者均可显著抑制脑片LTP的诱发率 ,并且PS增幅程度与对照组相比也显著降低 ,提示两者对海马LTP的诱生具有抑制作用。若用调心方 (7 4 5mg ml)与 β 淀粉样蛋白或皮质酮共同孵育脑片后 ,其LTP诱发率呈现上升趋势 ,同时PS增幅也显著提高。以上结果表明 ,调心方对 β 淀粉样蛋白或皮质酮对海马LTP的抑制效应具有明显的对抗作用 。 The effects of Tiao Xin Fang(TXF) on long term potentiation (LTP) in rat hippocampal slices pretreated with β amyloid or corticosterone were investigated by extracellular microelectrode recording technique.The results showed that the successful rate of evoking LTP was about 60% under normal condition.The PS amplitude was significantly increased and PS latent period was decreased.Pre incubation of hippocampal slices with β amyloid(0.2μM) or corticosterone(2μM) had little effect on either the sharp or amplitude of PS,indicating that they didn't influence the basal synaptic transmission.However,after tetanus the LTP induction rate and PS amplitude were both obviously decreased compared with the control,suggesting either of them inhibited LTP generation.In vitro application of TXF(7.45mg/ml) significantly antagonized their inhibitory effects on LTP induction.These results suggested that TXF antagonized the inhibitory effects of β amyloid and corticosterone on LTP in rat hippocampal slices and that may be one of the mechanisms of TXF in improving the impaired learning and memory function of Alzheimer's disease patients.
作者 万勤 张永祥
出处 《中国实验方剂学杂志》 CAS 2002年第6期22-25,共4页 Chinese Journal of Experimental Traditional Medical Formulae
基金 国家自然科学基金重点项目 (39830 4 50 )
关键词 调心方 LTP Β-淀粉样蛋白 皮质酮 海马脑片 Tiao Xin Fang long term potentiation β amyloid corticosterone hippocampal slices
  • 相关文献

参考文献5

二级参考文献10

共引文献72

同被引文献23

  • 1林水淼 杨柏灿.养心健脑液治疗Alzheimer痴呆的临床研究[J].上海中医药大学学报,1997,11(1):44-44.
  • 2O'Brien J T, Ames D, Schweitzer I, et al. Enhanced adrenal sensitivity of adrenocorticotrophic hormone (ACTH) is evidence of HPA axis hyperactivity in Alzheimer's disease [J].Psychol Med, 1996, 26(1): 7-14.
  • 3Magri F, Locatelli M, Baiza G, et al. Pathological brain aging [J]. Chronobiol Int, 1997, 14(4): 385-396.
  • 4Balldin J, Blennow K, Gottfries C G, et al. Relationship between mental impairment and HPA axis activity in dementia disorders [J]. Dementia, 1994, 5(5): 252-256.
  • 5Sapolsky R M. A mechanism for glucocorticoid toxicity in the hippocampus; increased neuronal vulnerability to metabolic insults [J]. J Neurosci, 1985, 5: 1228-1240.
  • 6Sapolsky R M. Pulsinelli W. Glucocorticoids potentiate ischemic injury to neurons: therapeutic implication [J].Science, 1985, 229: 1397-1401.
  • 7Bodnoff S R, Humphreys A G, Lehman J C, et al. Enduring effects of chronic corticosterone treatment on the spatial learning, synaptic plasticity, and hippocampal neuropathology in young and mid-aged rats [J].J Neurosci, 1995, 15(1): 61-69.
  • 8Tomita T,Maruyama K,Saido TC, et al.The presenilin 2 mutation (Nl411)linked to familial Alzheimer's disease(Volga German families) increases the secretion of amyloid beta protein ending at 42nd (or 43rd) residue.Proc Nad Acad Sci USA1997;94(5):2025-2030.
  • 9Selkoe DJ.Alzheimer's disease: genotypes,phenotypes and treatments. Science 1997;275(5300):630-631.
  • 10Ye L, Qiao JT.Suppressive action produced by β-amyloid peptide fragment 31-35 on longterm potentiation in rat hippocampus vs N-methyl-D-aspartate receptor independent:it's offset by ( - ) hyperzine A.Neurosci Lett 1999;275(3):187-190.

引证文献3

二级引证文献3

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