奎硫平和阿立哌唑对精神分裂症患者睡眠质量的影响

目的：了解急性期精神分裂症患者主观睡眠质量及奎硫平、阿立哌唑对患者主观睡眠质量的影响。方法：将符合国际疾病分类第10版精神分裂症诊断标准的患者68例,按入院的先后顺序分为奎硫平组34例和阿立哌唑组34例,用匹兹堡睡眠质量指数（PSQI）和睡眠状况自评量表（SRSS）进行主观睡眠评价,用阳性和阴性症状量表（PANSS）、简明精神病评定量表（BPRS）评定精神症状。用治疗中出现的症状量表（TESS）评定不良反应。结果：共57例完成研究。奎硫平组治疗前PSQI总分平均（11．81±4．81）分、治疗后（1．14±1．75）分;SRSS总分治疗前（32．16±7．13）分、治疗后（16．10±4．67）分。阿立哌唑组治疗前PSQI总分平均（10．97±5．28）分、治疗后（3．60±3．71）分;SRSS总分治疗前平均（29．73±7．31）分、治疗后（20．33±10．53）分。多元逐步回归分析显示,入组时PSQI总分、SRSS总分与PANSS分呈正相关（r=0．496,P=0．000;r=0．391,P=0．000）。结论：急性期精神分裂症患者主观睡眠质量降低,入睡时间延长,实际睡眠时间减少。经奎硫平或阿立哌唑治疗后,睡眠质量改善。     

急性期精神分裂症患者睡眠与血小板5-HT的关系

目的探讨急性期精神分裂症患者精神症状、睡眠质量与血小板5-HT浓度的关系。方法将符合入组标准的精神分裂症患者68例按入院的先后顺序分为喹硫平组34例和阿立哌哇组34例,用高效液相色谱仪（HPLC—ECD）在治疗前后测定血小板5-HT浓度,用匹兹堡睡眠质量指数（PSQI）和睡眠状况自评量表（SRSS）进行主观睡眠评价,用阳性和阴性症状量表（PANSS）、简明精神病评定量表（BPRS）评定精神症状。正常对照组30例。结果患者组治疗前5-HT浓度与对照组比较,差异无统计学意义（P〉0．05）,对照组、患者组治疗前后血小板5-HT浓度性别比较差异无统计学意义（P〉0．05）。多元逐步回归分析显示,患者组治疗前5-HT浓度与PSQI总分呈正相关（r=0．328,P=0．013）;治疗后5-HT浓度与病程、家族史、首次发病年龄呈正相关（r=0．422,P=0．001;r=0．522,P=0.000;r=0．575,P=0.000）;5-HT浓度变化率与治疗前PSQI因子分--日间功能、入睡时间及家族史、治疗前SRSS总分呈正相关（r=0．429,P=0．001;r=0．644,P=0．000;r=0．539,P=0．000;r=0．694,P=0．000）。结论血小板5-HT浓度在一定程度反映了中枢5-HT的功能,以血小板5-HT含量作为精神分裂症的生物学标记还有待于进一步探讨。     

老年抑郁障碍患者睡眠紊乱与抑郁疗效关系的一年随访研究北大核心CSCD

目的对住院治疗的抑郁障碍老年患者进行1年随访,分析睡眠紊乱与抑郁病情变化的关联,为临床实践中对老年患者的睡眠紊乱和抑郁症状进行合理处理提供参考。方法本研究为自然状态的观察研究,患者为符合ICD．10中抑郁发作、单次或复发性抑郁障碍诊断标准的住院患者,年龄≥60岁,共69例。采用匹兹堡睡眠质量指数（Pittsburgh Sleep Quality Index,PSQI）评估睡眠状况,总分〉18分为存在睡眠紊乱,采用HAMD、HAMA评估病情,MMSE评估认知功能。末次评估增加功能大体评定量表（Global Assessment Function,GAF）评估社会功能。在基线、治疗2周末、4周末及1年随访完成量表评估、记录药物治疗情况等,其中62例完成全部评估。采用重复测量方差分析和相关分析比较不同时点量表评分的变化及相关关系。结果患者在基线、治疗2周末、4周末和1年随访的PSQI得分分别为（15．4±3．8）、（12．0±4．6）、（9．4±4．3）、（8．5±4．7）分,重复测量方差分析显示,治疗2周末和4周末与基线相比减分率差异均有统计学意义（F=48．85、40．92,均P〈0．05）,治疗4周末与1年随访时差异无统计学意义（F=1．86,P=0．178）。有睡眠紊乱的患者2周末和4周末时联合使用镇静催眠药的比例更高。2周末PSQI减分率与2周末和4周末HAMD减分率正相关（r=0．33、0．40,均P〈0．05）,但与1年时HAMD减分率不相关（r=0．16,P〉0．05）。1年随访时仍存在的睡眠紊乱与HAMD评分正相关（OR=11．56,Waldχ2=4．26;P〈0．05）,与HAMA、MMSE和GAF评分无关联。结论老年抑郁障碍患者的睡眠紊乱在治疗早期改善可预示急性治疗期抗抑郁疗效较好,睡眠紊乱可随有效抗抑郁治疗而改善,治疗1年后仍存在睡眠紊乱更可能是抑郁障碍的残留症状。     

低频重复经颅磁刺激治疗精神分裂症顽固性幻听的临床研究

目的：研究左侧颞顶区低频（1Hz）重复经颅磁刺激（rTMS）治疗伴有顽固性言语性幻听的精神分裂症的疗效。方法：将35例伴有顽固言语性幻听的精神分裂症患者随机分为研究组18例和对照组17例。在原有抗精神病药种类及剂量不变的基础上,研究组给予左侧颞顶区频率为1Hz的真性rTMS刺激2周共10次,对照组给予相应的假性刺激。两组治疗前后均采用阳性与阴性症状量表（PANSS）评定其总体临床症状及幻听的变化,并进行威斯康星卡片分类测验（WCST）及听觉注意力测验（CPT）。结果：35例患者均完成治疗,研究组治疗前后幻听评分分别为（4．89±1．18）分和（3．00±1．75）分,对照组治疗前后幻听评分分别为（4．88±1．11）分和（4．24±1．20）分（F=7．72,P=0．009）。研究组有效率77．8％显著优于对照组41．2％（P=0．041）。治疗后两组问PANSS评分除阴性症状外其他各项评分改善差异均有显著性（P〈0．05）。WCST和CFF评分治疗后两组间差异无显著性（P〉0．05）。结论：左侧颞顶区rTMS对于幻听具有较肯定的治疗作用,并且能够改善精神分裂症患者的总体精神病性症状。在一定程度上能够改善患者的认知功能,但尚无确切疗效。     

综合干预对精神分裂症患者睡眠质量的影响

目的探讨综合干预对精神分裂症患者睡眠质量的影响。方法将符合《中国精神障碍分类与诊断标准(第3版)》(CCMD-3)的精神分裂症诊断标准以及伴有睡眠障碍的80例患者,采用"不平衡指数最小分配原则"分为研究组和对照组各40例。对照组只进行睡眠卫生健康教育,研究组接受睡眠卫生健康教育及音乐治疗、刺激控制、渐进性肌肉放松综合干预,疗程一个月。干预前后采用匹茨堡睡眠质量指数(PSQI)测定两组患者睡眠质量。结果干预前,对照组和研究组PSQI总评分分别为(9.70±1.65)分和(9.79±1.88)分,差异无统计学意义(P0.05)。干预后,研究组PSQI主观睡眠质量(1.43±0.68)、入睡时间(2.23±0.56)、睡眠持续性(0.83±0.67)、睡眠障碍(1.49±0.51)、习惯性睡眠效率(0.28±0.50)、日间功能障碍(1.04±0.59)评分及总评分均低于干预前,差异有统计学意义(P0.05)。对照组PSQI各项得分和总得分均高于研究组,差异有统计学意义(P0.05)。结论综合干预可能有助于改善精神分裂症患者的睡眠质量。     

曲唑酮治疗苯二氮革类药物依赖和戒断反应的临床对照研究

目的探讨曲唑酮对苯二氮革类药物依赖性失眠的疗效和安全性。方法共40例苯二氮革类药物依赖性失眠患者,分为苯二氮革类联合曲唑酮组（曲唑酮组）和苯二氮革类联合安慰剂组（对照组）,逐渐减半苯二氮革类药物剂量,治疗3个月后根据HoItzman—Gellert戒断症状评分法、汉密尔顿焦虑量表（HAMA）和多导睡眠图监测结果评价曲唑酮戒断疗效,副反应量表（TESS）评价药物不良反应。结果与对照组比较,曲唑酮组患者自治疗后7d戒断症状评分开始降低（P=0．000）,自治疗后15dHAMA评分开始降低（P=0．000）;与治疗前比较,经曲唑酮治疗后两项评分均降低（P=0．000）。与对照组比较,曲唑酮组患者治疗后7d总睡眠时间和慢波睡眠时间延长、睡眠效率提高、睡眠潜伏期缩短（均P=0．000）;与治疗前相比,经曲唑酮治疗后总睡眠时间和慢波睡眠时间延长、睡眠效率提高、睡眠潜伏期缩短（均P=0．000）。未见明显不良反应,两组患者治疗前后TESS评分差异无统计学意义（P〉0．05）。结论曲唑酮治疗苯二氮革类药物依赖和戒断反应疗效显著,且安全性良好。     

酸枣仁汤对失眠症疗效及血浆褪黑素水平的影响

目的探讨酸枣仁汤对失眠症的疗效及对血浆褪黑素水平的影响。方法选用酸枣仁汤治疗失眠症,采用匹兹堡睡眠质量指数（PSQI）量表评定睡眠状况,采用放射免疫法测定血浆褪黑素水平,观察其治疗前后的变化,并与正常对照进行比较,统计分析分别采用t检验、F检验和直线相关分析。结果治疗前患者PSQI总分明显高于正常对照组（f=3．282,P=0．002）,治疗后患者PSQI总分下降（r=2．371,P=0．007）;患者组治疗前、治疗后和正常对照组血浆MT水平分别为（45．81±13．23）pg／ml、（49．01±16．53）pg／ml和（54．86±18．35）pg／ml,组间比较有差异显著意义（F=5．004．P=0．009）,治疗前明显低于正常对照组和治疗后MT水平;治疗前MT水平与PSQI总分、睡眠质量因子分、入睡时间因子分分剐呈负相关关系（P〈0．05或P〈0．01）。结论酸枣仁汤治疗失眠有明显的疗效,其作用机制可能与MT水平调节有关。     

高频重复经颅磁刺激合并艾司西酞普兰治疗老年难治性抑郁症对照研究

目的 探讨高频重复经颅磁刺激（rTMS）合并艾司西酞普兰对老年难治性抑郁症的治疗价值和安全性.方法 将70例老年抑郁症患者随机分为研究组和对照组各35例,两组患者均服用艾司西酞普兰15 mg/d,疗程4周;研究组合并rTMS治疗.治疗前后使用汉密尔顿抑郁量表（HAMD）、贝克抑郁量表（BDI）、大体功能评定量表（GAF）及匹茨堡睡眠质量指数量表（PSQI）评定疗效.结果 研究组有效率高于对照组（x2=6.97,P＜0.01）.研究组治疗4周后GAF量表评分与治疗前比较显著升高（P＜0.01）,而BDI、HAMD、PSQI量表评分均明显下降（P＜0.01）;对照组治疗4周后HAMD、PSQI量表评分与治疗前比较明显下降（P＜0.01）.治疗后GAF量表研究组评分显著高于对照组（P＜0.01）;而BDI、HAMD、PSQI量表评分研究组显著低于对照组（P＜0.01）.结论 高频重复经颅磁刺激合并艾司西酞普兰治疗老年难治性抑郁症效果明显,无明显不良反应.     

劳拉西泮联合低频重复经颅磁刺激对慢性失眠障碍的效果

目的探讨劳拉西泮联合低频重复经颅磁刺激(rTMS)对慢性失眠障碍的临床疗效,为慢性失眠障碍的治疗提供参考。方法纳入符合《中国失眠障碍诊断和治疗指南》慢性失眠障碍诊断标准的患者120例,按照随机数字表法分为劳拉西泮联合低频rTMS治疗组(研究组)与劳拉西泮联合伪低频rTMS治疗组(对照组)各60例。于治疗前和治疗第4周末进行多导睡眠监测(PSG),于治疗前和治疗第1、2、4周末进行匹兹堡睡眠质量指数量表(PSQI)、汉密尔顿抑郁量表17项版(HAMD-17)和汉密尔顿焦虑量表(HAMA)评定。结果①治疗第4周末,研究组PSQI评分低于对照组(t=-3. 506,P=0. 001),研究组睡眠质量疗效的显效率和有效率均高于对照组(χ~2=4. 658、5. 926,P均0. 05);研究组实际睡眠总时间、睡眠效率均高于对照组(t=2. 333～3. 784,P均0. 05),睡眠潜伏期、觉醒时间、觉醒次数、快速眼球运动睡眠潜伏期均低于对照组(t=-2. 903～-2. 214,P均0. 05)。②治疗第4周末,研究组HAMA评分低于对照组(t=-2. 072,P0. 05);治疗第1、2、4周末,研究组HAMD-17评分均低于对照组(t=-2. 190～-1. 701,P均0. 05)。结论劳拉西泮联合低频rTMS可能有助于改善慢性失眠障碍患者的睡眠质量,并缓解其抑郁、焦虑等负性情绪。     

盐酸文拉法辛对慢性精神分裂症患者认知功能的影响

目的探讨盐酸文拉法辛对恢复期慢性精神分裂症患者认知功能障碍的影响。方法将疗效已达显著进步以上的62例慢性精神分裂症患者,随机分为研究组（32例）和对照组（30例）,在给予盐酸文拉法辛治疗前、后,对两组患者分别进行事件相关电位P埘检查及阳性症状与阴性症状量表（PANSS）评定,并进行分析。结果在治疗后,研究组P300靶刺激P3潜伏期缩短和波幅升高（P〈0．01）,PANSS评定提示阴性、反应缺乏及抑郁因子分下降和激活因子分升高（P〈0．01～0．05）,与对照组比较差异均有显著性意义（P〈0．01～0．05）。对照组治疗前后P300项目和PANSS评分比较差异均无显著性意义（P〉0．05）。结论盐酸文拉法辛对改善慢性精神分裂症患者的认知障碍是有裨益的。     

Environmental factors in the development and progression of late-onset Alzheimer＇s disease

Late-onset Alzheimer＇s disease （LOAD） is an age-related neurodegenerative disorder characterized by gradual loss of synapses and neurons, but its pathogenesis remains to be clarified. Neurons live in an environment constituted by neurons themselves and glial cells. In this review, we propose that the neuronal degeneration in the AD brain is partially caused by diverse environmental factors. We first discuss various environmental stresses and the corresponding responses at different levels. Then we propose some mechanisms underlying the specific pathological changes, in particular, hypothalamic-pituitary adrenal axis dysfunction at the systemic level; cerebrovascular dysfunction, metal toxicity, glial activation, and Aβ toxicity at the intercellular level; and kinase-phosphatase imbalance and epigenetic modification at the intracellular level. Finally, we discuss the possibility of developing new strategies for the prevention and treatment of LOAD from the perspective of environmental stress. We conclude that environmental factors play a significant role in the development of LOAD through multiple pathological mechanisms.     

高血压脑出血的显微外科治疗进展

高血压脑出血（Hypertensive intrac-rebral hemorrhage,HICH）是具有高发病率、高病死率、高致残率的急性脑血管疾病,占所有脑卒中患者的10%-20%,早期病死率可高达49.4%。随着人口老龄化,其发病率逐年提高;而外科手术的干预,使其病死率有所下降,但致残率居高不下。如何提高手术疗效和患者生存质量,一直是神经外科医师努力的方向。微侵袭血肿清除术因其手术创伤小,恢复快,是目前国内治疗高血压脑出血的重要手段。     

神经内镜联合亚低温治疗高血压基底节区脑出血

目的 探讨神经内镜联合亚低温在治疗高血压基底节区脑出血中的临床应用价值.方法 回顾性分析我院神经内镜治疗高血压基底节区脑出血患者40例的临床资料,并对治疗结果进行分析.结果 神经内镜治疗组22例(甲组),神经内镜联合亚低温治疗组18例(乙组),术后3个月根据GCS评分,甲组恢复良好1例,中残4例,重残6例,植物生存6例,死亡5例;乙组恢复良好4例,中残8例,重残3例,植物生存1例,死亡2例,两组比较差异有统计学意义(P＜0.05).两组颅内压比较第1天两者差异不明显,但第2、3天亚低温组颅内压明显降低.结论 神经内镜是治疗高血压基底节区脑出血较为有效的手术方式,联合亚低温治疗能有效降低颅内压,改善术后神经功能恢复,具有较好的临床应用价值.     

阻塞型睡眠呼吸暂停综合征患者情绪障碍的研究进展

在临床中睡眠呼吸暂停综合征患者患抑郁、焦虑的概率较高,而且同时患有抑郁、焦虑及OSAS的患者比仅患有OSAS患者病情更重。尽管许多研究评估了OSAS与情绪障碍间的关系,OSAS及情绪障碍之间一些可能的因果机制也已被提出,但是OSAS在情绪障碍的因果关系仍不清楚。对于OSAS伴焦虑抑郁状态的患者,情绪障碍的干预治疗有助于改善OSAS患者的嗜睡、疲劳症状及认知功能,提高患者生活质量。     

阿尔茨海默病治疗的研究进展

阿尔茨海默病（AD）是一种隐匿性起病,进行性恶化的神经退行性疾病,临床最初表现为认知功能障碍,并有可能在5～10年内完全衰退。患者往往伴随严重的记忆力丧失、精神行为异常、人格改变、言语功能障碍,无法独立生活,最终近乎于植物状态。Ferri等采用DISMOD软件在全球60岁以上人群中估计,全球的痴呆患者人数到2040年将达到8llO万左右。     

Total saponins of Panax ginseng effects on proliferation and differentiation of human embryonic neural stem cells and in a Parkinson’s disease mouse model

BACKGROUND： Total saponins of Panax ginseng （TSPG） exhibits neuroprotection against Parkinson＇s disease in the substantia nigra. OBJECTIVE： To investigate the effects of TSPG on human embryonic neural stem cells （NSCs） proliferation and differentiation into dopaminergic neurons using in vitro studies, and to observe NSC differentiation in a mouse model of Parkinson＇s disease, as well as behavioral changes before and after transplantation. DESIGN, TIME AND SETTING： In vitro neural cell biology trial and in vivo randomized, controlled animal trial were performed at the Institute of Basic Medical Sciences, Chongqing Medical University between September 2004 and December 2007. MATERIALS： TSPG （purity 〉 95%） was isolated, extracted, and identified by Chongqing Academy of Chinese Materia Medica. Recombinant human basic fibroblast growth factor （bFGF） and recombinant human epidermal growth factor （EGF） were purchased from PeproTech, USA. A total of 25 C57/BL6J mice, aged 18-20 weeks were included. Twenty were used to establish a Parkinson＇s disease model with i.p. injection of MPTP （1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine） and TSPG alone or combined with interleukin-1 （IL-1）-treated NSCs prior to transplantation into the corpus striatum. The remaining five mice were pretreated for 3 days with TSPG prior to MPTP injection, serving as the TSPG prevention group. METHODS： Primary NSCs were isolated, cultured and purified from embryonic cerebral cortex. Immunocytochemistry was employed to detect specific antigen expression in the NSCs. In vitro experiment： （1） to induce proliferation, NSCs were treated with TSPG, EGF＋bFGF, or TSPG＋EGF＋bFGF, respectively; （2） to induce dopaminergic neuronal differentiation, NSCs were treated with TSPG, IL-1, or TSPG＋IL-1, respectively. MAIN OUTCOME MEASURES： In vitro experiment： the effects of TSPG on NSCs proliferation were evaluated with flow cytometry and MTT assay. Tyrosine hydroxylase expression was determined by immunocytochemistry assay to observe effects of TSPG on dopaminergic neuronal differentiation. In vivo experiment： differentiation of grafted NSCs in the mouse brain was determined by immunohistochemical staining. Behavioral changes were evaluated by spontaneous activity frequency, memory function, and score of paralysis agitans. RESULTS： （1） NSCs were cultured and passaged for more than three passages. Immunocytochemistry revealed positive nestin staining, as well as neurofilament protein and glial fibrillary acidic protein. （2） TSPG significantly increased NSC proliferation, in particular when combined with EGF and bFGF, which was twice as effective as FGF or bFGF alone. TSPG also induced dopaminergic differentiation in NSCs, in particular when TSPG was added together with IL-1, resulting in an effect five times greater than that of IL-1 alone. （3） At day 30 following transplantation, most NSCs in the TSPG prevention group differentiated into dopaminergic neurons, and the scores of paralysis agitans, spontaneous activity, and memory function were significantly increased compared with TSPG alone or TSPG＋IL-1 groups （P 〈 0.05）. CONCLUSION： TSPG stimulated NSC proliferation, in particular when combined with FGF and bFGF. TSPG significantly induced dopaminergic neuronal differentiation of NSCs, and the effect was greater when combined with IL-1. In addition, TSPG greatly improved behavior in the Parkinson＇s disease mouse model following NSC transplantation. Following NSC transplantation, TSPG pretreatment exhibited superior efficacy over either TSPG alone or TSPG in combination with IL-1, in terms of behavioral improvements in the Parkinson＇s disease mouse model.     

Effects of p75 neurotrophin receptor knockout on axonal regeneration in a mouse model of facial nerve injury

BACKGROUND： Previous studies have shown that p75 neurotrophin receptor plays an important role in peripheral nerve injury. However, the role of p75 neurotrophin receptor in the regeneration of peripheral nerves remains poorly understood. OBJECTIVE： To study the effect of p75 neurotrophin receptor on facial nerve regeneration. DESIGN, TIME AND SETTING： A randomized controlled experiment was performed in the Regeneration Laboratory of Flinders University, Australia and the Biomedical Laboratory of Dentistry School, Shandong University from March 2005 to February 2006. MATERIALS： Cholera toxin B subunit, fast blue, and biotin rabbit-anti goat IgG were provided by Sigma, USA; goat-anti choleratoxin B subunit ant/body was provided by List Biologicals, USA. METHODS： In p75 neurotrophin receptor knockout and wild type 129/sv mice, the facial nerves on one side were crushed. At days 2 and 4 following injury, regenerating motor neurons in the facial nuclei were labeled by fast blue, and the regenerating axon was labeled by the anterograde tracer choleratoxin B subunit. MAIN OUTCOME MEASURES： Axonal regenerative velocity and number were detected by immunohistochemical staining of choleratoxin B subunit, growth-associated protein, protein gene product 9.5, and calcitonin-gene-related peptide; survival of motor neurons in the facial nuclei was detected by retrograde fast blue. RESULTS： Axonal growth in the facial nerve of p75 neurotrophin receptor knockout mice was significantly less than in wild type mice. At day 7 after injury, the number of regenerating motor neurons in p75 neurotrophin receptor knockout mice remained significantly less than in wild type mice （P 〈 0.05）. The number of positively stained fibers for growth-associated protein-43, protein gene product 9.5, and calcitonin-gene-related peptide in p75 neurotrophin receptor knockout mice was significantly less than in wild type mice （P 〈 0.01）. CONCLUSION： p75 neurotrophin receptor promoted axonal regeneration and enhanced the survival rate of motor neurons following facial nerve injury.     

墨蝶呤还原酶基因与精神分裂症相关性的研究进展

墨蝶呤还原酶（SPR）催化四氢生物蝶呤（BH4）从头合成途径的最后一步反应。SPR基因遗传缺陷或突变可导致BH。的合成紊乱,影响单胺类神经递质（如多巴胺、5-羟色胺及谷氨酸等）的合成或释放,进而参与包括精神分裂症在内的多种神经精神系统疾病的发生发展过程。此外,SPR基因敲除小鼠表现出持续增强的自主活动等类精神分裂症症状,说明该基因在精神分裂症的发病中扮演重要的角色。进一步研究SPR基因及其单核苷酸多态性的功能,可为阐明精神分裂症的发病机制提供重要的线索,也为新一代抗精神病药物的研制及开发开拓新的视野。现对SPR基因与精神分裂症的相关研究做一综述。     

Edema and neuronal apoptosis in the hippocampus and cortex of elderly rats following transient cerebral ischemia/reperfusion injury

BACKGROUND： Previous studies of cerebral ischemia have used young animals, with an ischemic time greater than 5 minutes （safe time limit）. Despite an increased understanding of neuronal apoptosis, it remains uncertain whether brief cerebral ischemic events of 5 minutes or less damage brain tissue in elderly rodents. OBJECTIVE： To investigate the effects of transient cerebral ischemia （5 minutes）/reperfusion injury on brain cortical and hippocampal edema, aquaporin-4 （AQP-4） expression, and neuronal apoptosis in aged rats, and to compare ischemic sensitivity between cortex and hippocampus. DESIGN, TIME AND SETTING： A randomized, controlled, animal experiment was performed at the Institute of Cerebrovascular Disease, Qingdao University Medical School from April 2008 to March 2009. MATERIALS： Rabbit anti-AQP-4 polyclonal antibody, TUNEL kit, and SABC immunohistochemistry kit were purchased from Wuhan Boster Bioengineering, China. METHODS： A total of 160 healthy, male, aged 19-21 months, Wistar rats were randomly assigned to 4 groups： sham-surgery, and ischemia 1-, 3-, and 5-minute groups, with 40 rats in each group. The global cerebral ischemia model was established using the Pusinelli four-vessel occlusion, and the three cerebral ischemia groups were subdivided into reperfusion 12-hour, 1-, 2-, 3-, and 7-day subgroups, with 8 rats in each subgroup. The sham-surgery group was subjected to exposure of the first cervical bilateral alar foramina and bilateral common carotid arteries. MAIN OUTCOME MEASURES： The dry-wet weight assay was used to measure brain water content and histopathology of the cortex and hippocampus was observed following hematoxylin-eosin staining. In addition, cortical and hippocampal AQP-4 expression was detected by streptavidin-biotin complex immunohistochemistry, and neuronal apoptosis was detected by the TUNEL method. RESULTS： There was no significant difference in brain water content or AQP-4 expression in the cortex and hippocampus between ischemia 1- and 3-minute groups and the sham-surgery group or brain water content or AQP-4 expression in the cortex between ischemia 5-minute group and sham-surgery group （P 〉 0.05）. However, brain water content and AQP-4 expression in the hippocampus after 5 minutes of cerebral ischemia were significantly increased compared with the sham-surgery group （P 〈 0.05 or P 〈 0.01）. Several TUNEL-positive cells were observed in the cortex and hippocampus of the sham-surgery group and ischemia 1-minute group, as well as in the cortex of the ischemia 3-minute group. In addition, the number of apoptotic neurons in the hippocampus of ischemia 3-minute group and in the cortex and hippocampus of ischemia 5-minute group was significantly increased （P 〈 0.05 or P 〈 0.01 ）. Neuronal apoptosis was increased after 12 hours of ischemia/reperfusion, and it reached a peak by 2 days （P 〈 0.01）. CONCLUSION： Transient cerebral ischemia （5 minutes） resulted in increased hippocampal edema, AQP-4 expression, and neuronal apoptosis. Moreover, cerebral ischemia had a greater effect on neuronal apoptosis than brain edema or AQP-4 expression, and the hippocampus was more sensitive than the cortex.