中国北方地区老年人冬季维生素D缺乏与骨量丢失**☆

背景：中国北方地区老年人维生素D营养状态存在季节变化,冬春季维生素D缺乏严重。 目的：分析沈阳市老年人冬季维生素D缺乏对骨量丢失的影响。 方法：随机选择沈阳市60岁以上汉族健康老年人100名,于2000-03检测受试者血浆中25羟维生素D、甲状旁腺激素、钙和磷,清晨空腹2 h尿中脱氧吡啶、钙、磷、肌酐,2000-03/2005-03两次检测髋部骨密度。 结果与结论：基线时,血浆25羟维生素D浓度为(31.0±12.30) nmol/L,40%受试者低于25 nmol/L;血浆甲状旁腺激素水平为(29.4±11.5) ng/L,血浆25羟维生素D浓度低于25 nmol/L者甲状旁腺激素水平为(34.6±13.5) ng/L,血浆25羟维生素D浓度与甲状旁腺激素呈负相关(r=-0.479,P < 0.000 1)。5年后股骨颈骨丢失率为(3.05±4.07)%,大转子为(1.46±5.02)%,经体质量和身高变化率校正后,股骨颈骨丢失率与基线血浆25羟维生素D浓度呈负相关(r=-2.3,P=0.02),股骨颈骨丢失率基线血浆25羟维生素D浓度≤ 25 nmol/L者高于浓度>25 nmol/L者103%( F=7.206 2,P=0.008 5)。其他检测指标与骨丢失无显著相关性。说明老年人群冬季维生素D缺乏严重,维生素D缺乏促进骨量丢失,影响骨健康。     

散发性重症肌无力患者267例维生素D受体基因多态性

目的 探讨中国汉族人维生素D受体(VDR)基因Fok Ⅰ和Apa Ⅰ位点多态性与重症肌无力(MG)的关系.方法 采用聚合酶链反应-限制性内切酶片段多态性(PCR-RFLP)法检测VDR基因Fok Ⅰ和Apa Ⅰ位点的多态性,比较基因型和等位基因在健康对照组及各MG亚组中的分布,并观察其与MG严重程度和激素短期疗效的关系.结果 Fok Ⅰ和Apa Ⅰ位点的基因型和等位基因频率在MG组和对照组间以及MG各亚组间的分布差异无统计学意义.Fok Ⅰ位点的基因型和等位基因频率在激素短期疗效好和疗效差组间的分布差异亦无统计学意义;但Apa Ⅰ位点的A等位基因频率在两组间差异有统计学意义,疗效好者(55/186,29.6%)高于疗效差者(7/48,14.6%,OR=2.46,95%CI 1.04～10 43,x2=4.400,P=0.036);激素短期疗效好者中携带基因型AA及Aa的频率(48/93,51.6%)高于疗效差者(7/24,29.2%,OR=2.59,95% CI 0.98～14.60,x2=3.858,P=0.049).结论 在我国汉族人散发性MG患者的VDR基因中,未发现Fok Ⅰ和Apa Ⅰ变异位点显著增加MG的患病风险,但携带Apa Ⅰ位点的A等位基因的MG患者激素短期疗效可能较好.

Abstract：

Objective To explore the associations between vitamin D receptor ( VDR) Fok- Ⅰ and Apa- Ⅰ polymorphisms and myasthenia gravis (MG) in Chinese Han population.Methods Polymorphisms of VDR Fok- Ⅰ and Apa-Ⅰ were determined by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method.The frequencies of genotypes and hyplotypes were compared among 286 normal controls and 267 MG patients in different subgroups classified by gender,age of onset,presence of thymoma,and Osserman classification sat maximal severity in the follow-up.The association between the genotypes and maximal severity of MG and short-term glucocorticoid treatment were also investigated.Results There were no significant differences in frequencies of genotypes and hyplotypes of both Fok-Ⅰ and Apa-Ⅰ between MG group and control group,and among subgroups of MG.The Fok- Ⅰ showed no statistical difference between the patients with better and less improvement after short-term treatment of glucocorticoid.The frequency of Apa-Ⅰ alleles in the patients with better improvement (55/186,29.6% ) significantly differed from the less improved group ( 7/48,14.6%,OR = 2.46,95% CI 1.04-10.43,x2 = 4.400,P = 0.036).The patients with the genotype A A/Aa were more likely to improve better after the treatment(48/93,51.6%) than in the worse group(7/24,29.2%,OR =2.59,95% CI 0.98-14.60,x2 =3.858,P= 0.049).Conclusions Alleles and genotypes of VDR-Fok- Ⅰ and Apa-Ⅰ were not found to be related with MG onset and severity.MG patients with VDR-Apa-A allele may have better improvement short-term treatment of glucocorticoid.     

Parkin基因多态性与帕金森病遗传易患性关系的研究

目的探讨Parkin基因S/N167和V/L380位点多态性与帕金森病遗传易患性的关系。方法以100例原发性帕金森病患者(其中40例为早发帕金森病患者)和100例健康体格检查者为研究对象。提取基因组DNA,采用聚合酶链反应方法扩增Parkin基因外显子4和外显子10,然后用内切酶AlwnI和Bsp1286I进行酶切,采用限制性酶切片段长度多态性的方法分析Parkin基因两个多态位点S/N167和V/L380等位基因与基因型频率分布差异。结果早发帕金森病患者S/N167多态位点等位基因A和含A基因型频率分布明显高于对照组(χ2=6.011,5.883;均P<0.05);帕金森病组和早发帕金森病组与对照组受试者的V/L380多态性等位基因和基因型频率分布相比,组间差异无统计学意义(χ2=0.884,1.023;均P>0.05)。结论Parkin基因S/N167多态性与帕金森病遗传易患性有关。     

降钙素受体基因多态性与原发性骨质疏松的相关性★

目的：骨质疏松是多基因调控疾病，峰值骨量达到和骨量丢失均受遗传因素影响。观察山东半岛地区汉族人群降钙素受体Alu-Ⅰ基因多态性各基因型频率及其与骨质疏松的关系，探讨原发性骨质疏松症的遗传易感因素。 方法：试验于2005-06/2007-06在青岛大学医学院附属医院中心实验室完成。①试验对象：选取332名长期居住在山东半岛地区无亲缘关系的汉族人群，纳入标准：健康门诊查体人员、原发性骨质疏松症及原发性骨质疏松症所致骨折患者；患者对试验知情同意。排除标准：各种继发性骨质疏松症；影响骨代谢相关疾病史；服用影响骨代谢药物等。其中骨质疏松合并骨折75例作为骨质疏松性骨折组，余257例经过骨密度测定确定骨量，按骨质疏松诊断标准（骨密度测定值比同性别峰值骨密度均值降低2.5个标准差）分为骨量正常组（n =201）及骨质疏松组（n =56）。②试验方法：应用聚合酶链反应限制性片段长度多态性分析技术测定257名山东半岛汉族成年人和75名骨质疏松性骨折患者降钙素受体基因型，用双能X射线吸收法测定腰椎、股骨颈、粗隆间、Ward’s三角和大转子区等部位的骨密度值。 结果：纳入受试者332人，均进入结果分析。①本试验人群降钙素受体基因型频率分布均符合Hardy-Weinberg 定律(χ2=0.47，P =0.493)。基因型频率分布依次为CC型占89.5%，CT型占10.5%，TT型占0%。②年龄与不同部位骨密度值之间呈负相关（P < 0.01），体质量指数与骨密度值之间呈正相关（P < 0.01），在将年龄和体质量指数进行校正后发现女性CC基因型较CT基因型在ward’s三角区有较高的骨密度（P < 0.05)，骨量正常组各基因型与骨质疏松性骨折组之间差异无显著性意义（P > 0.05)。 结论：山东半岛汉族女性降钙素受体基因型与骨密度之间存在一定关联，降钙素受体C1377T基因多态性可能成为胶东半岛汉族女性发生骨质疏松危险性的遗传标志。     

5-羟色胺2C受体基因启动子区多态性与迟发性运动障碍的关联分析

目的　探讨 5 羟色胺 2C(5 HT2C)受体基因启动区 - 759C/T和 - 697G/C单碱基置换多态性与精神分裂症伴迟发性运动障碍 (TD)的相关性。方法　先用异常不自主运动量表 (AIMS)评定精神分裂症男性患者有无TD及其严重程度 ,再对 42例符合TD(AIMS总分≥ 3分 )者和与TD组严格相匹配的 50例非TD者 ,采用简明精神病评定量表 (BPRS)评定精神症状 ,并应用聚合酶链反应 限制性片段长度多态性方法分析 5 HT2C受体基因的分布频率。结果　 (1 )TD组的 - 697C(突变型 )半合子型频率 (38% )高于非TD组 (1 8% ;χ2 =4 7,P =0 0 3 ,OR =2 8)。TD组 - 759T(突变型 )半合子型频率和 - 759T/ - 697C突变型单倍体频率虽高于非TD组 ,但差异均无显著性 (χ2 值分别为 2 9和 4 9,P =0 0 9)。 (2 )TD组的AIMS和BPRS评分分别为 (6 5± 1 8)分和 (51 2± 7 8)分 ,非TD组分别为 0分和(50 0± 7 3)分 ,差异无显著性 (P >0 0 5)。结论　 5 HT2C受体基因启动控制区的 - 697G/T单碱基置换突变可能是精神分裂症患者发生TD的易感因素之一     

维生素D受体基因多个位点多态性与绝经后妇女骨密度及骨转换生化标志物的关系

目的：观察维生素D受体基因BSMⅠ,TAQⅠ,APAⅠ多态性与绝经后妇女骨密度及骨转换生化标志物的相关性。 方法：①2007-01/2008-12从福州常住汉族人中随机检测绝经后妇女576例, 年龄48-84(62.17±6.37)岁。受试者均知情同意。②记录年龄、绝经年限、体质量指数和绝经后骨折情况。③双能X射线骨密度仪检测正位第2~4腰椎、左侧股骨颈、大转子和Ward s三角区骨密度。④PCR-RFLP技术检测维生素D受体基因BSMⅠ,TAQⅠ,APAⅠ多态性。⑤用酶联免疫吸附法检测骨转换生化标志物(血清骨钙素、血清骨碱性磷酸酶、尿吡啶啉和尿脱氧吡啶啉)。 结果：561例合格受试者进入结果分析。①维生素D受体基因BSMⅠ,TAQⅠ,APAⅠ多态性各基因型间骨密度比较差异无显著性意义(P > 0.05)。②维生素D受体基因BSMⅠ,TAQⅠ,APAⅠ多态性各基因型间骨转换生化标志物比较差异无显著性意义(P > 0.05)。③维生素D受体基因BSMⅠ,TAQⅠ,APAⅠ多态性各基因型间骨质疏松症发生率比较差异无显著性意义(P > 0.05)。④维生素D受体基因BSMⅠ,TAQⅠ,APAⅠ多态性各基因型间绝经后骨折发生率比较差异无显著性意义(P > 0.05)。 结论：维生素D受体基因BSMⅠ,TAQⅠ,APAⅠ多态性与绝经后骨质疏松症无明显关联,不能作为福州地区绝经后妇女骨质疏松的遗传标志。     

北京部分汉族男性维生素D受体基因Fok Ⅰ多态性与骨密度的关系

背景：骨质疏松症是受遗传和环境因素共同作用的多因子复杂疾病。维生素D受体基因多态性被认为是调控骨量的重要遗传因素,但在不同种族人群中的研究结果仍存在争议。 目的：观察维生素D受体基因Fok Ⅰ多态性与北京地区部分汉族男性骨密度的关系,以探求北京地区男性骨质疏松症的遗传易感性。 设计、时间及地点：随机对照试验,在2004-09/2007-12在解放军第二炮兵总医院内分泌科和解放军总医院老年病研究所分子生物学实验室共同完成。 对象：筛选2004-09/2006-12长期居住北京地区无血缘关系的20~80岁健康汉族男性230人。 方法：用聚合酶链反应-限制性片段长度多态性(PCR-RFLP)分析法检测受试者维生素D受体基因Fok Ⅰ基因型,使用双能X射线吸收测定法检测随机抽取的100例受试者腰椎和髋部的骨密度。 主要观察指标：①受试者年龄、身高、体质量。②受试者维生素D受体基因Fok Ⅰ基因型。③受试者L2~4椎体、股骨颈、大转子及Wards三角部位骨密度。 结果：受试者维生素D受体基因Fok Ⅰ的基因型及基因频率的分布为FF 36.96%,Ff 46.96%,ff 16.08%,符合Hardy-Weinberg定律;校正年龄、体质量、身高和体质量指数对骨密度的影响后,40~59岁年龄段男性ff基因型组骨密度较FF,Ff基因型低(P=0.037)。其余各年龄段、各部位ff基因型组骨密度大多低于FF,Ff基因型,但差异无显著性意义(P > 0.05)。 结论：北京地区汉族男性维生素D受体基因Fok Ⅰ多态性分型与骨密度之间可能存在一定关联,该项检测对筛查男性骨质疏松症高危人群的意义需进一步研究。     

中国汉族瘢痕疙瘩家系易感基因位点的定位分析

背景：转化生长因子β是目前与瘢痕关系最为密切的细胞因子，而SMAD蛋白介导的信号通路是转化生长因子β下游信号传递的主要途径。人SMAD蛋白基因在15q22.31-q23及18q21.1染色体区域。实验假定Smad基因为选择的瘢痕疙瘩家系易感基因位点。 目的：定位中国汉族瘢痕疙瘩家系的易感基因位点。 设计、时间及地点：两个家系、大样本的微卫星扫描连锁分析实验，于2007-02/06在上海基康公司实验室完成。 材料：选择6个国内不同地区的瘢痕疙瘩家系2个4代发病的NM、LN家系中32位和19位成员，严格遵照赫尔辛基宣言规定的准则采集血样和病理组织标本。 方法：采集2个家系51名成员的外周静脉血样，提取基因组DNA；选取位于15q22.31-q23及18q21.1染色体区域的7个微卫星标记位点D15S108 、D15S216、D15S534、D18S363、D18S460、D18S467、D18S846，对这些微卫星位点进行聚合酶链反应扩增，产物片断基因分型，再进行连锁分析。 主要观察指标：NM和LN瘢痕疙瘩家系外显率为90%时各位点LOD值。 结果：NM、LN两个瘢痕疙瘩家系在外显率分别为90%条件下，重组率θ=0~0.5时，这些微卫星标记的两点LOD值绝大部分都小于1，排除连锁关系存在。 结论：分析结果发现中国汉族瘢痕疙瘩家系易感基因位点不在染色体15q22.31-q23及18q21.1区域。     

血管内皮生长因子基因启动子区多态与散发性阿尔茨海默病的关系

目的 研究血管内皮生长因子(vascular endothelial growth factor,VEGF)基因启动子区多态与散发性阿尔茨海默病(sporadic Alzheimer's disease,SAD)发病的关系.方法 用聚合酶链反应.限制性片段长度多态性(PCR-RFLP)或直接测序的方法对北方汉族279例SAD患者和317名健康对照者进行多态分型.采用SPSS 11.5统计学软件包进行等位基因和基因型分布的比较及其与疾病的关联分析.结果 北方汉族人群中VEGF启动子存在3个多态位点:-2578C/A(rs699947)、-2549I/D(rs35569394)和-1154G/A(rs1570360),其中-2549I/D位点为18个碱基的插入或缺失.-2578C/A和-2549I/D存在显著的连锁不平衡,当-2578为A等位基因时,-2549I/D位点有18个碱基的插入,而当-2578是C纯合子时,-2549I/D位点则为18个碱基的缺失.这3个多态位点的基因型频率、等位基因频率以及单体型分布在SAD患者和对照组间差异无统计学意义.用Logistic回归校正年龄、性别和ApoE状态后,-1154G/A的GG基因型增加了SAD的发病风险.在不携带ApoE ε4的亚组中,单体型-2549D/-1154G可能增加SAD的发病风险(OR=1.325,95%CI1.023～1.716,P=0.033).结论 北方汉族人群中VEGF启动子存在3个多态位点-2578C/A、-2549I/D和-1154G/A.-1154G/A的GG基因型增加了SAD的发病风险.在不携带ApoE ε4的情况下,VEGF启动子的-2549D/-1154G单体型可能是SAD发病的危险因素.     

内脏素启动子区－3186C>T的单核苷酸多态性：非酒精性脂肪肝与正常人群的比较☆

目的：采用酶连接检测反应和基因芯片相结合的检测方法，检测东北地区汉族人群内脏素基因启动子区-3186 C>T的单核苷酸多态性（SNPs-3186 C>T），并分析其与非酒精性脂肪肝的相关性。 方法：选择2006-01/2007-05于吉林大学第一医院诊断明确的非酒精性脂肪肝患者79例，以及同期的健康体检者69例，运用酶连接检测反应和基因芯片相结合的方法，检测所有受试者的内脏素基因启动子区-3186 C>T的单核苷酸多态性，同时测量受试者的身高、体质量、腰围、臀围，并检测空腹胰岛素水平、肝功能、血糖、血脂等临床指标。所有受试者均为东北地区的汉族人,均签署了知情同意书。 结果：①CC, CT, TT基因型在非酒精性脂肪肝患者中分别为22.78%，50.63%，26.58%,在正常对照组中分别为21.74%，53.62%，24.64%。SNPs-3186 C>T的基因型频率和等位基因频率在两组中的分布差异无显著性(P > 0.05)。②非酒精性脂肪肝患者的SNPs-3186 C>T不同基因型的各测量指标及临床指标比较差异均无显著性(P > 0.05)。 结论：在东北地区汉族人中存在内脏素基因启动子区-3186 C>T的单核苷酸多态性，但与非酒精性脂肪肝无相关性。     

Detection of dopamine D2 receptor mRNA and binding sites in monkey amniotic epithelial cells.

Previous results from our laboratory showed that monkey amniotic epithelial cells (MAEC) possess the catecholamine synthesizing enzymes and have the capacity to synthesize and release CA. Recently, we also reported that these cells express dopamine D1 receptor mRNA and binding sites. This study was designed to investigate the presence of dopamine D2 receptors in MAEC. Using RT-PCR, we found that MAEC express dopamine D2 receptor mRNA that is having 98% homology with human dopamine D2 receptors. Radioligand saturation binding studies showed a 3H-YM-09151-2 high-affinity binding site with a K(D) of 0.293+/-0.06 nM and Bmax of 180.69+/-11.61 fmol/mg protein. Competition experiments with a variety of displacing drugs demonstrated that D2 antagonists potently compete with 3H-YM-09151-2 binding, whereas D1 antagonists displayed a weaker competition for the binding sites. The rank order of potency of these compounds in competing with 3H-YM-09151-2 for binding sites was consistent with the pharmacology of the dopamine D2 receptors. All competition curves were better fitted to a one-site model with a Hill coefficient around unity, indicating that 3H-YM-09151-2 is labeling a single population of receptors. These results provide, for the first time, a compelling evidence that MAEC natively express dopamine D2 receptor mRNA and binding sites, and they suggest that monkey amniotic epithelial cells (MAEC) could represent a source of primate dopamine receptors without the need for transformation or cloning procedures using nonprimate cells, as generally happens.     

Platelet serotonin-2 receptor binding sites in depression and suicide

In order to examine the role of serotonin-2 (5HT2) receptors in depression and suicide, we determined 5HT2 receptors using 125I-lysergic acid diethylamide (LSD) as the binding ligand in platelets obtained from 20 normal control and 23 drug-free depressed patients. Our results indicate significantly increased 125I-LSD binding sites (Bmax) in the platelets of depressed patients compared with normal control subjects. We also observed that a subgroup of depressed patients with a recent history of suicide attempts or suicidal ideation had significantly higher 5HT2 binding sites as compared with nonsuicidal depressed patients and normal controls. There were no significant differences in the apparent dissociation constant (Kd) values in the platelets of depressed patients compared with normal control subjects. To examine if the baseline 5HT2 receptors are related to either the severity of illness or treatment response, we determined the relationships of the baseline Bmax and Kd with baseline Hamilton Depression Rating Scale (HDRS) and Brief Psychiatric Rating Scale (BPRS) scores and change in scores after treatment. We found no significant correlation between baseline Bmax and Kd with the baseline HDRS or BPRS scores or change in these scores after psychoactive drug treatment. These results thus indicate increased platelet 5HT2 receptors in depression, but much more so in depressed patients with suicidal ideation or attempts.     

D2 receptor binding in dopa-responsive dystonia

We have studied dopamine D₂ receptor binding by [¹¹C]raclopride positron emission tomography in 14 patients with dopa-responsive dystonia (DRD). Data were compared with 16 levodopa-treated patients with Parkinson's disease (PD) and 26 healthy controls. The results revealed an elevated [¹¹C]raclopride binding index in the putamen and caudate nucleus of DRD patients compared with controls as well as significant elevation in the caudate nucleus compared with PD patients. The increase of [¹¹C]raclopride binding may be interpreted either as reduced tracer displacement by endogenous dopamine, or as an alteration of the receptor features due to chronic dopamine deficiency. The difference in [¹¹C]raclopride binding in DRD and PD patients in the caudate nucleus suggests that this structure may be of pathophysiological relevance in the presentation of the clinical features of both diseases.     

Postsynaptic localization of 5-HT1D receptor binding sites in human caudate

5-hydroxytryptamine1D (5-HT1D) receptor binding sites were quantified by saturation studies in the postmortem caudate nucleus and frontal cortex of individuals with Huntington's disease and control individuals with no known neurological disease. 3H-5-HT was used as the radioligand in the presence of 100 nM 8-OH-DPAT and 100 nM mesulergine in order to restrict radioligand binding to 5-HT1D receptors. No alteration in KD value was detected in Huntington's disease as compared to control brain tissue. However, the density (Bmax) of the 5-HT1D site was significantly decreased (P less than 0.01) in the caudate, but not the frontal cortex, of Huntington's disease versus control individuals. By contrast, no significant difference was found in Bmax or KD of [3H]paroxetine binding between control and Huntington's caudates. These data suggest that a significant number of caudate 5-HT1D receptors are located on the intrinsic neurons of the striatum as opposed to 5-HT nerve terminals.     

Postnatal development of dopamine D1 and D2 receptor sites in rat striatum

Tissue was obtained from corpus striatum of maturing rats at representative postnatal ages of 8-120 days for evaluation of D1 and D2 dopamine (DA) receptor sites in radioreceptor assays based on use of 0.05-2.5 nM concentrations of [3H]SCH-23390 or [3H]domperidone, respectively. Pharmacologic selectivity was verified by high rank-correlations (rs greater than 0.90) of Ki values for representative test agents in both assays (vs 0.3 nM ligand), using striatal tissue obtained at ages 20 and 120 days. Data from repeated (3-5x) six-concentration isotherm experiments involving a wide range of D1 or D2 radioligand concentrations were analyzed by linear regression of specific binding (B) vs free ligand concentration (F) in linearized form (B/F vs B) for each replicate assay and for pooled values, as well as by curve-fitting all available raw data (B vs F) using the LIGAND program adapted to microcomputer. Values for apparent ligand affinity (Kd = 0.15-0.35 nM) failed to show a consistent change with age, while values for apparent receptor site density (Bmax) followed a similar developmental course with both methods of analysis (between methods: r = 0.99 and 0.89 for D1 and D2 assays, respectively, across all ages tested).(ABSTRACT TRUNCATED AT 250 WORDS)     

Serotonin-2 binding sites in human frontal cortex and hippocampus. Selective loss of S-2A sites with age

Serotonin (S-2) binding sites were characterized in human frontal cortex and hippocampus throughout the lifespan. We found that the S-2 binding sites (labeled by [3H]spiperone and displaced by ketanserin) consisted of two subtypes (S-2A and S-2B) which are discriminated by competition with methysergide. The total S-2 sites in frontal cortex had a Bmax of 360 fmol/mg protein, which is approximately twice that of the hippocampus (160 fmol/mg protein). The density of total S-2 sites decreased with age in the frontal cortex of normal adults (17-100 years, n = 24). The receptor loss was primarily in the S-2A subclass. This loss of S-2A sites occurred primarily after 60 years and decreased to 50% of young adult values by the 10th decade. In the hippocampus, S-2A binding sites decreased with age, but no effects on total S-2 or S-2B sites were detected. A study of infant brains suggested the S-2A subtype in frontal cortex increases postnatally. However, in the infant hippocampus the S-2 binding approximated adult levels.     

Brain 5-HT2 receptor binding sites in depressed suicide victims

5-HT2 receptor binding sites were measured (by saturation binding of [3H]ketanserin) in brain tissue obtained at postmortem from 19 suicide victims with definite evidence of depression and 19 sex and age-matched control subjects. Five of the suicide victims were receiving antidepressant drugs prior to death; 13 suicide victims had not been prescribed antidepressant or other psychoactive drugs recently and none were found in their blood at postmortem. The number of serotonin-2 (5-HT2) binding sites in frontal, temporal and occipital cortex and amygdala did not differ significantly between the depressed suicide victims and controls, either in the total suicide group or in the antidepressant drug-free suicides. The number of 5-HT2 binding sites in the hippocampus did not differ from controls in the total suicide group but was significantly lower (by 23%) in the antidepressant-free suicide group. The affinity of [3H]ketanserin binding did not differ from controls in the antidepressant-free suicides but was lower (increased Kd) in those subjects receiving antidepressant drugs. No correlation was found between the time of death and storage of tissue or the duration of tissue storage prior to assay and the number or affinity of 5-HT2 binding sites. A significant negative correlation was found between age of the subject and the number of 5-HT2 binding sites in the frontal and occipital cortex. The present study of suicide victims with definite evidence of depression do not confirm previous studies of increased numbers of 5-HT2 binding sites in suicide victims and suggest that these previous findings may be related to factors other than depression.