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26S蛋白酶复合体介导的蛋白降解对LTP产生的影响 被引量：2

Effects of 26S proteasome mediated protein degradation on the induction of LTP
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摘要 目的 :观察 2 6S蛋白酶复合体介导的蛋白降解对大鼠海马LTP产生的影响。 方法 :利用 2 6S蛋白酶复合体特异抑制剂和本室制备的 2 6S蛋白酶复合体抗体灌流海马脑片 ,观察海马CA1区通路LTP的诱导情况。 结果 :正常情况下 ,LTP诱出率为 86 %。在 2 6S蛋白酶复合体抗体灌流脑片情况下 ,LTP诱出率显著下降 (18% ) ;在 2 6S蛋白酶复合体特异抑制剂lactacystin存在条件下 ,LTP诱出率也明显降低 (0 % )。结论 :本研究证明 2 6S蛋白酶复合体抗体及特异抑制剂能显著抑制LTP产生。这提示 ,2 6S蛋白酶复合体介导的蛋白降解过程在LTP中发挥了重要作用。 Objective: To investigate if 26S proteasome mediated protein degradation affects the induction of long term potentiation (LTP). Methods: The induction of LTP in CA1 region of rat hippocampus in vitro was observed in the presence of the proteasome inhibitor and anti 26S proteasome antibody prepared in our lab. Results: The rate of LTP induction was 86% under the normal condition. When slices were perfused with anti 26S proteasome antibody, the rate of LTP induction decreased significantly (18%). In the presence of lactacystin (an inhibitor of 26S proteasome), the rate of LTP induction lowered markedly (0%). Conclusion: The anti 26S proteasome antibody and the proteasome inhibitor could reduce markedly the induction of LTP. It is indicated that 26S proteasome mediated protein degradation plays an important role in LTP induction. \[
作者 胡志安 谭银玲 罗峻 黎海蒂 蔡文琴 李希成
机构地区 第三军医大学基础医学部生理学教研室 第三军医大学基础医学部微生物学教研室 第三军医大学基础医学部神经生物学教研室
出处 《中国神经科学杂志》 CSCD 2003年第4期234-237,共4页
基金 国家自然科学基金资助项目 ( 3 960 0 0 48 3 0 2 70 44 3 )
关键词 26S蛋白酶复合体 蛋白降解 LTP 长时程增强 大鼠 海马 突触传递长时程增强 海马 S proteasome protein degradation long term potentiation plasticity rat
分类号 R33 [医药卫生—人体生理学]
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参考文献15

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同被引文献26

  • 1Gerlai R. Hippocampal LTP and memory in mouse strains: is there evidence for a causal relationship? Hippocampus 2002; 12 (5) :657 - 666.
  • 2Muller D, Nikonenko I, Jourdain P, Alberi S. LTP,memory and structural plasticity. Curr Mol Med 2002;2(7) :605 -611.
  • 3Tomimatsu Y, Idemoto S, Moriguchi S, Watanabe S, Nakanishi H. Proteases involved in long-term potentiation. Life Sci 2002 ;72 (4-5): 355 - 361.
  • 4Lu X, Wyszynski M, Sheng M, Baudry M. Proteolysis of glutamate receptor-interacting protein by calpain in rat brain: implications for synaptic plasticity. J Neurochem 2001 ;77(6) :1553 - 1560.
  • 5Akaishi T, Shiomi T, Sawada H, Yokosawa H. Purification and properties of the 26S proteasome from the rat brain: evidence for its degradation of myelin basic protein in a ubiquitin-dependent manner. Brain Res 1996; 722:139 - 144.
  • 6Hegde AN, DiAntonio A. Ubiquitin and the synapse.Nat Rev Neurosci 2002 ;3 ( 11 ) :854 - 861.
  • 7Chain DG, Schwartz JH, Hegde AN. Ubiquitin-mediated proteolysis in learning and memory. Mol Neurobiol 1999;20(2-3): 125 - 142.
  • 8Hegde AN, Inokuchi K, Pei W, Casadio A, Ghirardi M, Chain DG, Martin KC, Kandel ER, Schwartz JH.Ubiquitin C-terminal hydrolase is an immediate-early gene essential for long-term facilitation in Aplysia. Cell 1997 ;89 ( 1 ) :115 - 126.
  • 9Lopez-Salon M, Alonso M, Vianna MR, Viola H, Mello e Souza T, Izquierdo I, Pasquini JM, Medina JH. The ubiquitin-proteasome cascade is required for mammalian long-term memory formation. Eur J Neurosci 2001;4( 11 ) :1820 - 1826.
  • 10Ehlers MD. Activity level controls postsynaptic composition and signaling via the ubiquitin-proteasome system.Nat Neurosci 2003 ;6(3) :231 -242.

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中国神经科学杂志
2003年 第4期

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