神经性厌食症的生物学机制与临床意义.docVIP

神经性厌食症的生物学机制与临床意义 摘要 研究表明，遗传学与神经生物学的介导机制对神经性厌食症（AN）的病因起到重要影响。5-羟色胺神经系统Abstract Recent evidence suggests that genetic and neurobiologically mediated mechanisms contribute to the etiology of anorexia nervosa (AN). Serotonin neuronal systems, in particular, may create vulnerabilities related to pathological feeding, anxiety and obsessions, and extremes of impulse control, that make individuals susceptible to developing an eating disorder, perhaps in combination with environmental stressors. 关键词 神经性厌食症（AN） 5-羟色胺在过去十年中，一些证据提出了一种可能5-羟色胺的神经通路可能导致神经性厌食症（AN）的病理生理首先，的生理和药理研究表明，发生5-羟色胺活动的后。5-羟色胺神经系统5-羟色胺神经系统神经递质系统具有复杂的相互作用它可能5-羟色胺5-羟色胺神经元的胞体位于中线和脑干中缝核皮质，纹状体边缘地区。如脑成像技术和遗传学人类生活行为的关系营养不良夸大这些症状，因为确定这样的症状是否一后果或病理摄食行为或营养不良潜在原因是该领域主要方法问题。在发病前-羟色单胺类神经递质和神经肽的级联调节进食速度，饱足感，等等。5- HT1A自身受体或突触1B / D或2C受体焦虑（尤其是强迫症和社交恐怖症）体育健身活动，奖励和物质锥体上的树突棘和GABA能抑制性黑质纹状体和mesocorticolimbic的DA神经元产生黑质和腹侧被盖喂养，气质个性，身体，认知，锻炼身体考虑1. Kaye W, Strober M, Jimerson D. The neurobiology of eating disorders. In: Charney DS, Nestler EJ, editors. The neurobiology of mental illness. New York: Oxford Press; 2004. p 1112. 2. Brewerton TD, Brandt HA, Lessem MD, et al. Serotonin in eating disorders. In: Coccaro EF, Murphy DL, editors. Serotonin in major psychiatric disorders. Progress in psychiatry. Washington, DC: American Psychiatric Press, Inc; 1990. p 155. 3. Jimerson DC, Wolfe BE, Metzger ED, et al. Decreased serotonin function in bulimia nervosa. Arch Gen Psychiatry 1997; 54:529. 4. Walsh BT, Devlin MJ. Eating disorders: progress and problems. Science 1998;280:1387. 5. Steiger H, Young SN, Kin NM, et al. Implications of impulsive and affective symptoms for serotonin function in bulimia nervosa. Psychol Med 2001;31:85. 6. Cooper JR, Bloom FE, Roth RH. The biochemical basis of neuropharmacology. 7th edn. New York: Oxford University Press; 1996. 7. Frank GK, Kaye WH, Meltzer CC, et al. Reduced 5-HT2A receptor binding after recovery from anorexia nervosa. Biol Psychiatry 2002;52:896. 8. Bailer UF, Price JC, Meltzer CC, et al. Al