期刊文献+

抗抑郁药的信号转导机制 被引量:10

Signal transduction mechanism of antidepressant action
下载PDF
导出
摘要 抗抑郁药的作用机制目前尚不明确 ,传统单胺递质理论和受体理论都不能充分解释抗抑郁药的临床效应滞后现象。近年提出抗抑郁药的信号转导机制 ,认为抗抑郁药是以G蛋白为分子基础 ,神经递质受体和G蛋白为作用环节 ,最终影响细胞内的信号转导并产生磷酸化作用增加、神经营养因子增多、神经发生增加等相关效应 ,从而发挥抗抑郁作用。影响细胞内信号转导并产生相关效应需要的时间 ,与抗抑郁药的临床效应滞后时间相吻合 ,从而使抗抑郁药的滞后现象有了合理解释。这个机制的提出有助于抗抑郁新药的发展 ,为研制安全、有效的新药指明了方向 ,同时也为抑郁症生物学病因的阐明提供了必要信息。 The mechanisms of antidepressants are still unclear. There a re two classical theories on monoamine neurotransmitter or on neurotransmitter rec eptors, but both of them can not fully explain the delayed therapeutic action of antidepressants. Recently, many researches have focused on the postreceptor int racellular signal transduction as the mechanism of antidepressant action. G protein is the molecular basis of antidepressants. Neurotransmitter receptors and G protein are the two sectors of their therapeut ic action. They will ultimately influence intracellular signal transduction and result in relative effects such as phosphoration, the induction of neurotrophic factors and neurogenesis. This mechanism suggests a reasonable explanation for t he clinical delaying of antidepressants and it will do great help for the develo pment of antidepressants. It makes the design of novel, safe and more efficaciou s antidepressants possible and provides significant information for the elucidat ion of biology of depression.
出处 《中国临床药理学与治疗学》 CAS CSCD 2004年第12期1321-1326,共6页 Chinese Journal of Clinical Pharmacology and Therapeutics
关键词 抗抑郁药 信号转导 环磷酸腺苷 G蛋白 Β-肾上腺素受体 antidepressants signal transduction cAMP G proteins β-adrenergic receptor
  • 相关文献

参考文献20

  • 1[1]Donati RJ, Thukral C, Rasenick MM. Chronic treatment of C6 glioma cells with antidepressant drugs results in a redistribution of Gsalpha[J]. Mol Pharmacol, 2001;59(6):1426-32
  • 2[2]Simbrey K, Winterhoff H, Butterweck V. Extracts of St.John's wort and various constituents affect β-adrenergic binding in rat frontal cortex[J]. Life Sci, 2004; 74(8):1027-38
  • 3[3]Burgi S, Baltensperger K, Honegger UE. Antidepressant-induced switch of beta 1-adrenoceptor trafficking as a mechanism for drug action[J]. J Biol Chem, 2003;278(2):1044-52
  • 4[4]Zill P, Jager M, Rupprecht R, Moller HJ, Ackenheil M, Bondy B, et al. Beta-1-adrenergic receptor gene in major depression: influence on antidepressant treatment response[J]. Am J Med Genet, 2003; 120B(1):85-9
  • 5[5]Gonzalez-Maeso J, Rodriguez-Puertas R, Meana JJ, Garcia-Sevilla JA, Guimon J. Neurotransmitter receptor-mediated activation of G proteins in brains of suicide victims with mood disorders: selective supersensitivity of alpha(2A)-adrenoceptors[J]. Mol Psychiatry, 2002; 7(7):755-67
  • 6[6]Subhash MN, Nagaraja MR, Sharada S, Vinod KY. Cortical alpha-adrenoceptor downregulation by tricyclic antidepressants in the rat brain[J]. Neurochem Int, 2003; 43(7):603-9
  • 7[7]Rogoz Z, Margas W, Skuza G, Solich J, Kusmider M, Dziedzicka-Wasylewska M. Effect of repeated treatment with reboxetine on the central alpha 1-adrenergic and dopaminergic receptors[J]. Pol J Pharmacol, 2002; 54(6):593-603
  • 8[8]Bourin M, David DJ, Jolliet P, Gardier A. Mechanism of action of antidepressants and therapeutic perspectives[J]. Therapie, 2002; 57(4):385-96
  • 9[9]Van Oekelen D, Luyten WH, Leysen JE. 5-HT2A and 5-HT2C receptors and their atypical regulation properties[J]. Life Sci, 2003; 72(22):2429-49
  • 10[10]Dremencov E, Gispan-Herman I, Rosenstein M, Mendelman A, Overstreet DH, Zohar J, et al. The serotonin-dopamine interaction is critical for fast-onset action of antidepressant treatment: in vivo studies in an animal model of depression[J]. Prog Neuro Psychopharmacol Biol Psychiatry, 2004; 28(1):141-7

同被引文献174

引证文献10

二级引证文献63

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