|本期目录/Table of Contents|

[1]陈文博,寇亚芬,张引国,等.贝沙罗汀拮抗Aβ25-35诱导的海马CA1区锥体神经元谷氨酸能突触传递的抑制效应[J].天津医科大学学报,2017,23(04):285-289.
 CHEN Wen-bo,KOU Ya-fen,ZHANG Yin-guo,et al.Antagonistic effect of bexarotene on Aβ25-35 -Induced inhibiting action in glutamatergic synaptic transmission of hippocampal CA1 pyramidal neurons[J].Journal of Tianjin Medical University,2017,23(04):285-289.
点击复制

贝沙罗汀拮抗Aβ25-35诱导的海马CA1区锥体神经元谷氨酸能突触传递的抑制效应(PDF)
分享到:

《天津医科大学学报》[ISSN:1006-8147/CN:12-1259/R]

卷:
23卷
期数:
2017年04期
页码:
285-289
栏目:
基础医学
出版日期:
2017-07-02

文章信息/Info

Title:
Antagonistic effect of bexarotene on Aβ25-35 -Induced inhibiting action in glutamatergic synaptic transmission of hippocampal CA1 pyramidal neurons
文章编号:
1006-8147(2017)04-0285-05
作者:
陈文博1寇亚芬2张引国3赵景霞1张 玲1
(1.天津医科大学生理学与病理生理学系,天津 300070;2.天津医科大学一中心临床学院放射科,天津 300192;3.武警后勤学院生理学与病理生理学教研室,天津300309)
Author(s):
CHEN Wen-bo1 KOU Ya-fen2 ZHANG Yin-guo3 ZHAO Jing-xia1 ZHANG Ling1
(1. Department of Physiology and Pathophysiology, Tianjin Medical University, Tianjin 300070, China; 2. Department of Radiology, The First Center Clinic College, Tianjin Medical University, Tianjin 300192, China; 3. Department of Physiology and Pathophysiology, Logistics University of Chinese People’s Armed Police Force, Tianjin 300309, China)
关键词:
阿尔茨海默病β淀粉样蛋白贝沙罗汀自发性兴奋性突触后电流微小性兴奋性突触后电流
Keywords:
Alzheimer’s disease amyloid beta-protein Bexarotene spontaneous excitatory postsynaptic currents miniature excitatory postsynaptic currents
分类号:
R338.8
DOI:
-
文献标志码:
A
摘要:
目的:初步探讨β淀粉样蛋白Aβ25-35损伤海马CA1区兴奋性突触的靶点及贝沙罗汀的可能拮抗效应。方法 以出生7~14 d Wistar大鼠海马脑片为研究对象,采用全细胞膜片钳技术,在电压钳模式下记录大鼠海马脑片CA1区锥体细胞自发兴奋性突触后电流(sEPSCs)和微小兴奋性突触后电流(mEPSCs),并分析不同组神经元sEPSCs和mEPSCs幅度及频率的差异。结果:与对照组相比,经Aβ25-35(1 μmol/L)处理后,海马神经元sEPSCs与mEPSCs平均幅度和平均频率都显著降低(均P< 0.05)。向Aβ25-35处理过的海马脑片中加入贝沙罗汀(5μmol/L)后,sEPSCs与mEPSCs平均幅度和平均频率较Aβ25-35组都显著提高(均P< 0.05)。贝沙罗汀处理组sEPSCs与mEPSCs平均频率和平均幅度与对照组水平已无显著性差异(均P> 0.05)。结论:25-35可作用于CA1区,导致海马锥体神经元兴奋性突触后电位降低,造成突触功能损伤,而贝沙罗汀通过作用于突触前和突触后位点拮抗Aβ25-35的损伤效应。
Abstract:
Objective: To explore the damage effect target of?? Aβ25-35??on hippocampal CA1 excitatory synapses and the possible antagonistic effect of bexarotene. Methods: Postnatal 7-14-day-old Wistar rats were used as the research subjects. Using a whole-cell patch clamp technique, and in voltage-clamp mode, we recorded spontaneous excitatory postsynaptic currents (sEPSCs) and miniature excitatory postsynaptic currents (mEPSCs) of CA1 pyramidal neurons in hippocampal slices. The changes of the amplitude and frequency of the sEPSCS and mEPSCs in each group were analyzed. Results: After Aβ25–35 (1 umol/L) application, the average amplitude and frequency of sEPSCs and mEPSCs were significantly reduced compared with the control group (P< 0.05). Following application of bexarotene (5 umol/L) to Aβ25-35 group, the average amplitude and frequency of sEPSCs and mEPSCs were significantly increased compared with the Aβ25–35 group(P< 0.05); and compared with the control group, the difference was not statistically significant (P> 0.05). Conclusion: 25-35 has a damage effect on CA1 pyramidal neurons, resulting in the decrease of excitatory postsynaptic potential and synaptic function damage, while bexarotene has a presynaptic and postsynaptic site of action to antagonize Aβ25-35-induced synaptic dysfunction in hippocampal CA1 pyramidal neurons.

参考文献/References:

[1] Masuzzo A, Dinet V, Cavanagh C, et al. Amyloidosis in retinal neurodegenerative diseases[J]. Front Neurol, 2016, 7:127

[2] Querfurth H W, Laferla F M. Alzheimer’s Disease [J]. N Engl J Med, 2010, 362(4): 329

[3] 李靖,付雪斐,孙凤仙,等.β片层阻断肽H102对双转基因AD模型小鼠脑内LPL和PPAR-γ表达的影响[J].天津医科大学学报,2016,22(5):396

[4] Wang D B, Kinoshita Y, Kinoshita C, et al. Loss of endophilin-B1 exacerbates Alzheimer’s disease pathology[J]. Brain, 2015, 138(7):2005

[5] 王冰艳,孙凤仙,林来祥,等.β片层阻断肽H102对PAP小鼠脑内ERK信号转导通路的影响[J].天津医药,2014,42(7):650

[6] Tomiyama T, Matsuyama S, Iso H, et al. A mouse model of amyloid beta oligomers: their contribution to synaptic alteration, abnormal tau phosphorylation, glial activation, and neuronal loss in vivo[J]. J Neurosci, 2010, 30(14): 4845

[7] Cramer P E, Cirrito J R, Wesson D W, et al. ApoE-directed therapeutics rapidly clear β-amyloid and reverse deficits in AD mouse models[J]. Science, 2012, 335(6075): 1503

[8] Kwon B, Gamache T, Lee H K, et al. Synergistic effects of β-amyloid and ceramide-induced insulin resistance on mitochondrial metabolism in neuronal cells[J]. Biochim Biophys Acta, 2015,1852(9): 1810

[9] 袁小涌,王超,孙凤仙,等.β片层阻断肽H102对双转基因AD小鼠突触可塑性相关蛋白的影响[J].中国应用生理学杂志,2016,32(4):293

[10] Edgar J R, Willén K, Gouras G K, et al. ESCRTs regulate amyloid precursor protein sorting in multivesicular bodies and intracellular amyloid-β accumulation[J]. J Cell Sci, 2015, 128(14): 2520

[11] Jawed S I, Myskowski P L, Horwitz S, et al. Primary cutaneous T-cell lymphoma (mycosis fungoides and Sezary syndrome): part II. Prognosis, management, and future directions[J]. J Am Acad Dermatol, 2014, 70(2): 223.

[12] Zhaowei L, Yongling X, Jiajia Y, et al. The reduction of EPSC amplitude in CA1 pyramidal neurons by the peroxynitrite donor SIN-1 requires Ca2+ influx via postsynaptic non-L-type voltage gated calcium channels[J]. Neurochem Res, 2014, 39(2): 361

[13] Yuan C, Zhang Y, Zhang Y, et al. Effects of ketamine on neuronal spontaneous excitatory postsynaptic currents and miniature excitatory postsynaptic currents in the somatosensory cortex of rats[J]. Iran J Med Sci, 2016, 41(4): 275

[14] Hsieh H, Boehm J, Sato C, et al. AMPAR removal underlies Abeta-induced synaptic depression and dendritic spine loss[J]. Neuron, 2006, 52(5): 831

[15] Tang B, Luo D, Yang J, et al. Modulation of AMPA receptor mediated current by nicotinic acetylcholine receptor in layer I neurons of rat prefrontal cortex[J]. Sci Rep, 2015, 5:14099

[16] 林杭,孙梅琴,张涛,等.不同阿片受体激动剂对海马培养神经元微小兴奋性突触后电流的影响[J].中国临床神经科学, 2010,18(1):10

相似文献/References:

[1]姜明月,于敏,李文,等.叶酸对N2a-APP695细胞Tau蛋白及其Ser396位点磷酸化的调控[J].天津医科大学学报,2013,19(05):365.
[2]付雪斐,李 靖,孙凤仙,等.β片层阻断肽对AD模型小鼠学习记忆及PI3K/AKT信号通路的影响[J].天津医科大学学报,2016,22(05):391.
 FU Xue-fei,LI Jing,SUN Feng-xian,et al. Effect of β-sheet breaker peptide on learning and memory and PI3K /AKT? signaling pathway in AD model mice ? [J].Journal of Tianjin Medical University,2016,22(04):391.
[3]孙凤仙,徐淑梅.H102-BD经鼻腔给药后对双转基因AD小鼠行为学及脑内APP和Aβ蛋白表达的影响[J].天津医科大学学报,2017,23(05):385.
 SUN Feng-xian,XU Shu-mei.Effect of H102-BD on behavior and the expression of APP and Aβ in PAP double transgenic AD mice after intranasal administration[J].Journal of Tianjin Medical University,2017,23(04):385.
[4]孙晓倩 综 述,吴 伟 审 校.睡眠剥夺与中枢神经系统疾病关系的研究进展[J].天津医科大学学报,2018,24(05):461.
[5]王晨旭 综述,于泳浩,谢克亮,等.AMPA受体在阿尔兹海默症中的研究进展[J].天津医科大学学报,2020,26(03):292.
[6]司蕊豪,刘羽茜,朱仲康,等.基于生信分析对阿尔茨海默病炎症相关关键基因的筛选及鉴定[J].天津医科大学学报,2023,29(05):486.
 SI Rui-hao,LIU Yu-xi,ZHU Zhong-kang,et al.Screening and identification of key genes associated with Alzheimer′s disease inflammation based on bioinformatics analysis[J].Journal of Tianjin Medical University,2023,29(04):486.

备注/Memo

备注/Memo:
基金项目 国家自然科学基金资助项目(81271224);天津市自然科学基金资助项目(15JCYBJC25400);教育部留学回国人员科研启动基金资助项目

作者简介 陈文博(1991-),男,硕士在读,研究方向:生理学;

通信作者: 张玲,E-mail: zhanglsl@tmu.edu.cn; 赵景霞,zhaojingxia@tmu.edu.cn
更新日期/Last Update: 2017-06-30