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TREK-1钾通道介导的抗抑郁及神经保护作用 被引量:2

The antidepressant and neuroprotective effect mediated by TREK-1 potassium channel
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摘要 目的系统分析TREK-1的结构功能及发挥这-作用的相关机制,以期为临床疾病的治疗提供新思路。方法计算机检索Medline/PubMed、CNKI、CBM及万方数据库中关于TREK-1及相关抗抑郁及神经保护的文献,提取TREK-1钾通道的结构功能及生理药理学相关介绍以及潜在的抗抑郁及神经保护作用机制相关研究,并对纳入文献的参考文献进行查询,检索期限为建库至2015年10月。结果文章最终纳入文献30篇,涉及TREK-1结构分布及调控因素的有14篇,TREK-1介导的抗抑郁研究13篇。TREK-1发挥神经保护作用的研究7篇。综上研究发现阻断或抑制TREK-1钾通道活性,产生显著的抗抑郁作用;激活该通道可扩张局部脑血管,抑制异常活跃放电的神经元。结论TREK-1钾通道在体内的抗抑郁及脑保护作用的研究已取得重要进展,下-步的研究应聚焦在探讨不同脑区TREK.1的最佳激活比例,以获得临床上抗抑郁及神经保护效果的最佳平衡。 Objective Recently, the role of TREK-1 in anti-depression and neuroprotection was demon- strated definitely. In this paper,a systematic review about the functional structure of TREK-1 as well as the under- lying mechanisms which involved in depression resistance and nerve protection was made for purpose of providing new ideas for the treatment of clinical diseases. Methods The electronic search of Medline/PubMed, CNKI, CBM and Wanfang Data were performed to collect the introduction of TREK-1 and the studies of depression and nerve protection in which TREK-1 participated from inception of each database to October 2015, besides the relevant ref- erences of the included studies were also retrieved. Results 30 studies were included in this paper. 14 studies were about the interpretation of TREK-I's structure, distribution and the regulatory factors,and the number of re- searches regarding the involvement of TREK-1 in anti-depression and neuroprotection was 13 and 7 respectively. Based on these studies, it was easily to conclude that inhibition or blocking of TREK-1 channels can produce obvi- ous antidepressant effect ,however,activation of TREK-1 channels will induce the dilation of local cerebral vascular and silence hyperactive neurons. Conclusion Some achievements about the antidepressant and neuroprotective effect of TREK-1 channels in vivo have been made gratifyingly,thus future research should focus on exploring the best TREK-lactivation ratio in different brain regions to gain the best balance between anti-depression and neuro- protection.
出处 《中华行为医学与脑科学杂志》 CAS CSCD 北大核心 2015年第12期1144-1146,共3页 Chinese Journal of Behavioral Medicine and Brain Science
基金 国家自然科学基金项目(31371074)
关键词 TREK-1 抑郁障碍 脑卒中 癫痫 TREK- 1 Depressive disorder Stroke Epilepsy
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参考文献30

  • 1Honore E. The neuronal background K2P channels:focus on TREK1 [ J ]. Nat Rev Neurosci, 2007,8 (4) : 251-261.
  • 2Dedman A, Sharif-Naeini R, Folgering JH, et al. The mechano-gated K (2P) channel TREK- 1 [ J ]. Eur Biophys J,2009,38 (3) : 293-303.
  • 3Fink M, Duprat F, Lesage F, et al. Cloning, functional expression and brain localization of a novel unconventional outward rectifier K+ chan- nel [ J ]. EMBO J, 1996. 15 (24) : 6854-6862.
  • 4Lesage F, Lazdunski M. Molecular and functional properties of two- pore-domain potassium channels [ J ]. Am J Physiol Renal Physiol, 2000,279(5) :F793-801.
  • 5Hervieu GJ, Cluderay JE, Gray CW, et al. Distribution and expression of TREK-I, a two-pore-domain potassium channel, in the adult rat CNS[J]. Neuroscience,2001,103(4) :899-919.
  • 6Talley EM, Solorzano G, Lei Q, et al. CNS distribution of members of the two-pore-domain (KCNK) potassium channel family [ J ]. J Neu- rosci, 2001,21 (19) : 7491-7505.
  • 7Blondean N, Petrault O, Manta S, et al. Polyunsaturated fatty acids are cerebral vasodilators via the TREK-1 potassium channel[ J] .Circ Res, 2007,101 (2) : 176-184.
  • 8La JH, Schwartz ES, Gebhart GF. Differences in the expression of tran-sient receptor potential channel V1, transient receptor potential chan- nel A1 and mechanosensitive two pore-domain K channels between the lumbar splanchnic and pelvic nerve innervations of mouse urinary bladder and colon [ J ]. Neuroscience, 2011,186 : 179-187.
  • 9Wang M, Song J, Xiao W, et al. Changes in lipid-sensitive two-pore domain potassium channel TREK-1 expression and its involvement in astrogliosis following cerebral ischemia in rats [ J ]. J Mol Neurosci, 2012,46(2) :384-392.
  • 10Magloire H,Maurin JC,Couble ML,et al. Topical review. Dental pain and odontoblasts:facts and hypotheses[ J ]. J Orofac Pain,2010,24(4) :335-349.

二级参考文献51

  • 1陈双庆,蔡庆,沈玉英,赵中,周华.轻度认知功能损害患者扣带后回谷氨酸多体素氢质子磁共振波谱研究[J].中华诊断学电子杂志,2013,1(1). 被引量:33
  • 2刘萍.抑郁症非药物治疗概况[J].中国行为医学科学,2006,15(2):186-187. 被引量:5
  • 3潘玉芹,林文娟.海马5-羟色胺系统与抑郁症[J].中国行为医学科学,2006,15(4):379-380. 被引量:28
  • 4Fava M,Kendler KS. Major depressive disorder. Neuron,2000,28:335-341.
  • 5Chen TJ,Yu YW,Hong CJ,et al. Association analysis for the C-1019G promoter variant of the 5-HT1A receptor gene with auditory evoked potentials in major depression. Neuropsychobiology ,2004,50:292-295.
  • 6Den Boer JA. Looking beyond the monoamine hypothesis. European Neurological Disease ,2006,32:2-3.
  • 7Svennirlgsson P,Chergui K,Rachleff I,et al. Aherations in 5-HT1B receptor function by p11 in depression-like states. Science,2006,311:77-80.
  • 8Tsai SJ. The P11, tPA/plasminogen system and brain-derived neurotrophic factor: Implications for the pathogenesis of major depression and the therapeutic mechanism of antidepressants. Medical Hypotheses, 2007, 68 : 180-183.
  • 9Santarelli L, Saxe M, Gross C, et al. Requirement of hippocampal neuregenesis for the behavioral effects of antidepressants. Science, 2003, 301:805-809.
  • 10Gage FH. Mammalian neural stem ceils. Science, 2000,28: 1433- 1438.

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同被引文献32

  • 1O'Leary OF, Dinah TG, Cryan JF. Faster, better, stronger : towards new antidepressant therapeutic strategies [ J ]. Eur J Pharmacol, 2015,753:32-50. DOI: 10. lO16/j.ejphar.2014.07.046.
  • 2Montgomery SA, Nielsen RZ, Poulsen LH, et al. A randomised, double-blind study in adults with major depressive disorder with an inadequate response to a single course of selective serotonin re- uptake inhibitor or serotonin-noradrenaline reuptake inhibitor treat- ment switched to vortioxetine or agomelatine [ J ]. Hum Psychophar-maeo1,2014,29 ( 5 ) :470-482. DOI : 10.1002/hup.2424.
  • 3Blum SI, Tourkodimitris S, Ruth A. Evaluation of functional health and well-being in patients receiving levomilnacipran ER for the treatment of major depressive disorder [ J ]. J Affect Disord, 2015, 170:230-236. DOt : 10.1016/j.jad.2014.09.005.
  • 4Asnis GM, Henderson MA. Levomilnacipran for the treatment of major depressive disorder: a review [ J ]. Neuropsyehiatr Dis Treat, 2015,11 : 125-135. DOI : 10.2147/NDT.S54710.
  • 5Learned S, Craft O, Roychowdhury S, et al. Efficacy, safety, and tolerability of a triple reuptake inhibitor GSK372475 in the treat- ment of patients with major depressive disorder: two randomized, placebo- and active-controlled clinical trials[J]. J Psychopharma- col, 2012,26 ( 5 ) : 653 -662. DOI : 10.1177/0269881111424931.
  • 6Wang Y, Chang T, Chen YC, et al. Quetiapine add-on therapy im- proves the depressive behaviors and hippocampal neurogenesis in fluoxetine treatment resistant depressive rats[ J]. Behav Brain Res, 2013,253:206-211. DOI : 10.1016/j.bbr.2013.07.021.
  • 7Lenze EJ, Mulsant BH, Blumberger DM, et al. Efficacy, safety, and tolerability of augmentation pharmacotherapy with aripiprazole for treatment-resistant depression in late life : a randomised, double- blind, placebo-controlled trial [ J ]. Lancet, 2015, 386 ( 10011 ) : 2404-2412. DOI : 10.1016/S0140-6736 ( 15 ) 00308-6.
  • 8Tamayo JM, Pica-Ruiz Y, Ruiz I. Olanzapine and fluoxetine com- bined as therapy for treatment-resistant depression: a systematic review[ J]. Arch Neurocien ,2015,20( 1 ) : 17-33.
  • 9Abbasi SH, Hosseini F, Modabbernia A, et al. Effect of celecoxib add-on treatment on symptoms and serum IL-6 concentrations in patients with major depressive disorder: randomized double-blind placebo-controlled study [ J ]. J Affect Disord, 2012, 141 (2-3) : 308-314. DOI: 10.1016/j.jad.2012.03.033.
  • 10Gallagher P J, Castro V, Fava M, et al. Antidepressant response in patients with major depression exposed to NSAIDs : a pharmacovig- ilance study [ J]. Am J Psychiatry 2012 159 (10) : 1065-1072. DOI: 10.1176/appi.ajp.2012.11091325.

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