中文摘要：

目的探讨5-羟色胺2A受体（5-HT2A）基因T102C多态性与抑郁症患者大脑灰质密度的相关性。方法以1.5T超导型磁共振仪对57例抑郁症患者及37名性别、年龄、受教育年限与患者组无差异的正常对照进行脑部的三维磁共振扫描,同时检测受试者的5-HT2A受体基因T102C多态性。采用基于像素的形态学分析方法分析被试的脑灰质图,建立方差分析（校正P〈0.005）模型以比较不同组间灰质密度差异,体素为10及以上（K≥10）的脑区为差异有统计学意义。结果患者组与对照组T102C多态性的基因型和等位基因频率差异均无统计学意义（P〉0.05）。CC基因型患者组左楔叶、左丘脑、右后扣带回灰质密度较TC基因型组降低（校正P〈0.005）,同时左右后扣带回、右额中回灰质密度也较TT基因型患者组降低（校正P〈0.005）;TC基因型患者组左扣带回灰质密度较TT基因型组降低（校正P〈0.005）。包括对照组不同基因型组在内的其他各组间未发现各脑区灰质密度存在差异（校正P〈0.005）。结论 5-HT2A受体C等位基因可能参与了抑郁症后扣带回等脑区结构异常的病理机制。

英文摘要：

Objective To explore the correlation of 5-hydroxytryptamine 2A receptor（5-HT2A） gene T102C polymorphism and the concentration of gray matter in patients with major depressive disorder and healthy participants.Methods Fifty-seven patients with depression,as well as 37 gender-,age-,education-matched healthy controls,underwent brain structural magnetic resonance imaging（3D） using 1.5T nuclear magnetic resonance imaging.Genotypes of 5-HT2A gene T102C polymorphism were detected using polymerase chain reaction-restriction fragment length polymorphism（PCR-RFLP） method.The concentration of grey matter in different genotype groups were compared using analysis of variance（corrected P〈0.005） after voxel-based morphometry（VBM） analysis.Cluster size ≥10 voxels（K≥10） was used to determine significant difference.Results There were not significant differences in the frequencies of genotype and alleles between the depressed group and the healthy group（P〈0.05）.In the patient group,CC genotype carriers had reduced concentration of grey matter（GMC） in the left cuneus,left thalamus and right posterior cingulated gyrus than the carriers of TC genotype（corrected,P〈0.005）.In addition,CC genotype carriers also had reduced concentration of GMC in the bilateral posterior cingulated gyrus and right middle frontal gyrus than TT genotype carriers（corrected,P〈0.005）.GMC in left cingulated gyrus was lower significantly in carriers of TC genotype than in carriers of TT genotype（corrected,P〈0.005）.Conclusions C allele of 5-HT2A receptor gene T102C polymorphism may contribute to the pathomechanism of abnormality in brain structure including posterior cingulate in patients with major depressive disorder.