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| 海马长时程增强与26S蛋白酶复合体活性变化的关系 | |
| 引用本文： | Hu ZA,Tan YL,Luo J,Li HD,Li XC. 海马长时程增强与26S蛋白酶复合体活性变化的关系[J]. 生理学报, 2003, 55(6): 648-652 |
| 作者姓名： | Hu ZA Tan YL Luo J Li HD Li XC |
| 作者单位： | 1. 第三军医大学基础医学部生理教研室,重庆,400038;第三军医大学基础医学部神经生物教研室,重庆,400038 2. 第三军医大学基础医学部微生物教研室,重庆,400038 3. 第三军医大学基础医学部生理教研室,重庆,400038 |
| 基金项目： | This work was supported by the National Natural Science Foundation of China ( No. 39600048 , 30270443) ) |
| 摘 要： | 实验观察了大鼠海马脑片上突触传递长时程增强(long term potentiation,LTP)的产生和维持中26S蛋白酶复合体活性的动态变化过程,初步分析了介导其变化的受体途径。结果显示:强直刺激前,26S蛋白酶复合体活性为190±14.3 cpm/(100 μg·2 h),强直刺激诱导fEPSP斜率增加10 min时,其活性升为273±18.3 epm/(100μg·2 h),强直刺激诱导fEPSP斜率增加60 min时,26S蛋白酶复合体活性又降为210±12.8 cpm/(100μg·2 h)。NMDA受体特异阻断剂AP-5在损害L1P产生的同时,抑制26S蛋白酶复合体活性升高。实验结果提示:大鼠海马LTP产生过程中,26S蛋白酶复合体活性存在一个短时间的,依赖于N-methyl-D-aspartate(NMDA)受体的升高过程。 |
| 关 键 词： | 长时程增强 蛋白酶复合体 N-methyl—D—aspartate（NMDA）受体 海马 大鼠 |
| 修稿时间： | 2003-03-04 |
Relationship between hippocampal long term potentiation induction and activity of 26S proteasome |
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| Hu Zhi-An,Tan Yin-Ling,Luo Jun,Li Hai-Di,Li Xi-Cheng. Relationship between hippocampal long term potentiation induction and activity of 26S proteasome[J]. Acta Physiologica Sinica, 2003, 55(6): 648-652 | |
| Authors: | Hu Zhi-An Tan Yin-Ling Luo Jun Li Hai-Di Li Xi-Cheng |
| Affiliation: | Department of Physiology,Third Military Medical University, Chongqing 400038. zhianhu@yahoo.com.cn |
| Abstract: | The present study examined the changes in 26S proteasome activity and the signal molecule mechanism regulating 26S proteasome activity in long term potentiation (LTP) in rat hippocampal slices. The results are as follows: 26S proteasome activity was 190+/-14.3 cpm/(100 microg.2 h) before tetanus, a significant increase in 26S proteasome activity (273+/-18.3 cpm/(100 microg.2 h) was found 10 min after tetanus, when the slope of fEPSP was markedly increased. Interestingly, 26S proteasome activity returned to baseline level (210+/-12.8 cpm/(100 microg.2 h) 60 min after tetanus. Moreover, the N-methyl-D-aspartate (NMDA) receptor inhibitor AP-5, which blocked LTP, prevented the increase in the 26S proteasome activity. The results suggest that NMDA receptors contribute to the transient increase in 26S proteasome activity during induction of LTP in the hippocampal CA1 region. |
| Keywords: | long term potentiation proteasome N-methyl-D-aspartate ( NMDA) receptors hippocampus rats |
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