针刺对缺血再灌注大鼠海马脑源性神经营养因子mRNA的影响

目的 探讨针刺对缺血再灌注大鼠海马内脑源性神经营养因子（BONF）基因表达的影响，推测针刺改善缺血再灌注的可能机制。方法 采用4-血管阴断法制备大鼠全脑缺血再灌注模型，电针刺激百会、肾俞、足三里穴后，利用RT-PCR检测BDNF mRNA。结果 正常组大鼠海马BDNF mRNA表达极低，缺血再灌注组大鼠海马BDNF mRNA表达明显增高，治疗15d的针刺1、2组大鼠海马BDNF mRNA表达较缺血再灌注组更高，及早治疗且治疗时间为20d的针刺3组大鼠海马BDNF mRNA表达较降低。结论 缺血再灌注大鼠海马BDNF水平增高有利于损伤的神经元存活、恢复；针刺促进脑内细胞分泌内源性BDNF可能是针刺有效治疗缺血再灌注的机制之一。     

氟西汀对卒中后抑郁大鼠海马脑源性神经营养因子表达的影响

目的 分析卒中后抑郁（post-stroke depression，PSD）模型大鼠海马脑源性神经营养因子（Brainderived neurotrophic factor，BDNF）蛋白及mRNA表达水平，及抗抑郁剂氟西汀干预后BDNF表达水平的变化，初步探讨BDNF在PSD发生中的作用。方法 大脑中动脉阻塞（Middle cerebral artery occlusion，MCAO）法建立局灶脑缺血模型，加用慢性不可预见温和应激（Chronic unpredictable mild stress，CUMS）结合孤养，建立PSD大鼠模型，并予以氟西汀干预。应用蛋白免疫印迹（Western-blot）、Real time-PCR分别检测应激18、28 d时海马BDNF蛋白及mRNA表达水平。结果 与对照组相比，应激14d后PSD组较对照组大鼠体重与糖水消耗比例降低，水平、垂直试验得分下降（P <0.05或P <0.01）。氟西汀干预组糖水消耗比例，水平、垂直试验得分均较PSD组显著增加（P <0.05或P <0.01）。第18、28天，PSD组BDNF蛋白水平较对照组均显著下降（P <0.05或P <0.01）。PSD组BDNF mRNA的表达在应激18d时较正常组有下降趋势，但无统计学意义；至28 d时，表达含量明显下降，差异有统计学意义（P <0.01）。第18、28天，氟西汀干预组BDNF蛋白及mRNA水平均较PSD组显著增加（P <0.01）。结论 应用MCAO模型联合CUMS加孤养模型制备的PSD大鼠模型在神经功能缺损的同时，表现快感缺乏和探索行为减少的抑郁核心症状，并且体重的增长幅度显著减慢。PSD大鼠海马BDNF蛋白及mRNA表达水平显著降低，氟西汀干预后BDNF表达水平上升，初步提示BDNF在卒中后抑郁发生中的作用。     

雌激素对脑卒中后抑郁大鼠海马和杏仁核脑源性生长因子-磷酸化酪氨酸激酶B表达以及行为学的影响

目的通过观察雌激素对缺血性脑卒中后抑郁大鼠模型海马和杏仁核的脑源性生长因子(BDNF)-磷酸化酪氨酸激酶B(pTrkB)的表达,探讨缺血性脑卒中后内源性抑郁的发病机制。方法将SD雌性大鼠随机分为对照组12只(无任何干预)、模型组16只(MCAO术后2周,皮下注射大豆油,持续2周)和雌激素组16只(MCAO术后2周,皮下注射溶有10μg 17β-雌二醇的0.1 mL大豆油,持续2周)。通过旷场实验和强迫游泳实验观察大鼠行为学变化,应用免疫组化和Western blot方法观察海马和杏仁核中BDNF和pTrkB表达。结果雌激素干预后:①旷场实验和强迫游泳中,大鼠行为学评分均显著提高,雌激素组与模型组比较,差异有统计学意义(P0.01);②免疫组化法观察示雌激素组海马和杏仁核BDNF阳性细胞数与模型组比较明显增多,差异有统计学意义(P0.05);③Western blot法检测示雌激素组BDNF/β-actin和pTrkB/TrkB灰度比值较模型组明显提高(P0.05)。结论雌激素能改善脑卒中后大鼠的抑郁行为,其机制可能是通过BDNF-pTrkB信号通路的变化而改善PSD症状。     

远志总皂苷对阿尔茨海默病模型大鼠海马脑源性神经营养因子及酪氨酸蛋白激酶B表达的影响

目的观察远志总皂苷对阿尔茨海默病模型大鼠海马CA1区脑源性神经营养因子(BDNF)及其特异性受体酪氨酸蛋白激酶B(TrkB)表达的影响,探讨远志总皂苷对阿尔茨海默病的干预作用机制。方法雄性Wistar大鼠被随机分为生理盐水组(正常对照组)、阿尔茨海默病模型组(模型组),以及远志总皂苷低剂量(12.50 mg/ml)和高剂量(37.50 mg/ml)组;采用D-半乳糖致衰老联合鹅膏覃氨酸损毁基底前脑Meynert核法建立阿尔茨海默病大鼠模型,免疫组织化学染色检测大鼠海马CA1区BDNF及其受体TrkB表达水平。结果 BDNF和TrkB阳性物质呈棕黄色,主要表达于海马CA1区神经元胞膜。模型组大鼠海马CA1区BDNF及其受体TrkB表达水平为0.30±0.02和0.21±0.07,低于正常对照组的0.47±0.02和0.46±0.05(均P=0.000);与模型组相比,远志总皂苷低剂量组(0.35±0.05,0.32±0.07)和高剂量组(0.43±0.05,0.37±0.03)大鼠海马CA1区BDNF及其受体TrkB表达水平均显著升高(均P=0.000),但以高剂量组升高更为显著(均P=0.000)。结论远志总皂苷可以显著升高阿尔茨海默病模型大鼠海马CA1区BDNF及其受体TrkB表达水平,且具有剂量依赖性,这可能是其改善认知功能的机制之一。     

高压氧预处理对异氟醚所致中年小鼠认知障碍的改善作用及海马脑源性神经营养因子和胶质细胞源性神经营养因子表达水平的影响

目的 探讨高压氧预处理对异氟醚（ISO）所致中年小鼠认知障碍的改善作用及海马 脑源性神经营养因子（BDNF）和胶质细胞源性神经营养因子（GDNF）蛋白表达和mRNA 水平的影响。 方法 将32 只8 月龄雄性C57BL/6J小鼠按随机数字表随机分为对照组（sham组）、高压氧组（HBO 组）、异 氟醚组（ISO 组）和高压氧预处理+ 异氟醚组（HBO+ISO 组），每组8 只。HBO 组和ESPS+HBO 组小鼠置于 高压氧舱进行1 h 高压氧（2.5 个大气压，100% O2）干预，对照组小鼠常压空气干预（模拟除压力和氧浓度 以外的其他过程和环境条件）1 h，均连续5 d。在第3 天HBO 或常压空气干预结束后2 h，各组小鼠进行 水迷宫训练，连续3 d。最后1 次水迷宫训练后24 h，ISO 组和HBO+ISO 组小鼠经异氟醚吸入麻醉构建认 知障碍模型，其他2 组吸入对照气体。24 h后进行水迷宫检测认知功能，并通过蛋白免疫印迹（Western Blot）和实时定量聚合酶链式反应（RT-PCR）检测小鼠海马BDNF和GDNF蛋白表达和mRNA水平的变化。 结果 （1）各处理组水迷宫总运动距离和平均运动速度的差异均无统计学意义（均P＞ 0.05）；ISO 组目标 象限停留时间百分比为（26.74±10.52）%，显著低于sham 组［（48.33±9.18）%，P ＜ 0.01］，而HBO+ISO 组 ［（39.06±8.39）%］则显著高于ISO 组（P ＜ 0.05）。（2）ISO 组海马BDNF（0.56±0.09）和GDNF（0.52±0.10） 的蛋白相对表达水平均显著低于sham组和HBO+ISO 组（均P ＜ 0.01 或0.05）。（3）ISO 组海马BDNF （0.51±0.08）和GDNF（0.25±0.09）的mRNA 相对水平也均显著低于sham 组和HBO+ISO 组（均P ＜ 0.01）。 （4）sham组与HBO 组在上述行为和分子水平之间的差异均无统计学意义（均P＞ 0.05）。结论 高压氧预 处理可能通过调节海马的BDNF 和GDNF表达水平，改善异氟醚所致认知损伤。     

更正:远志总皂苷对阿尔茨海默病模型大鼠海马脑源性神经营养因子及酪氨酸蛋白激酶B表达的影响

<正>由于第一作者陈伟荣个人疏忽,特申请将我刊2014年第14卷第5期"远志总皂苷对阿尔茨海默病模型大鼠海马脑源性神经营养因子及酪氨酸蛋白激酶B表达的影响"[1]一文脚注"作者单位:030032太原,山西医学科学院山西大医院神经内科"改为"作者单位:030001太原,山西医科大学研究生院2011级(陈伟荣,燕毅男,崔红丽);030032太原,山西医学科学院山西大医院神经内科(李新毅)",英文作者名"CHEN Wei-rong,YAN Yi-nan,CUI Hong-li,LI Xin-yi"改为"CHEN Wei-rong1,YAN Yi-nan1,CUI Hong-li1,LI Xin-yi2",英文单位"Department of Neurology,Shanxi Da Yi Hospital,Shanxi Academy of Medical Sciences,     

脑源性神经营养因子对脑梗死大鼠神经细胞凋亡及Bcl-2、Bax蛋白表达的影响

目的 探讨侧脑室内立体定向注射脑源性神经营养因子(BDNF)对脑梗死大鼠神经细胞凋亡及Bcl-2、Bax蛋白表达的影响.方法 32只SD大鼠成功制作大脑中动脉闭塞模型,随机分为BDNF组(n=16)和对照组(n=16),在两组大鼠侧脑室内分别注射10μ1 BDNF溶液(0.5 μmol)和10μl磷酸盐缓冲液(PBS液).注射2周后,2组大鼠分别行神经功能严重性评分(mNSS)及梗死面积测定,应用免疫组化染色、Western blot分析脑组织Bcl-2、Bax蛋白的表达,Tunel检测细胞凋亡.结果 与对照组比较,BDNF组脑梗死面积缩小,神经细胞凋亡数少,Bax蛋白表达低,Bcl-2蛋白表达高,短期内神经功能恢复好,差异均具有统计学意义(P＜0.05).结论 BDNF可能通过调节Bcl-2、Bax蛋白表达,减少神经细胞凋亡,改善脑缺血大鼠的功能.     

人参皂甙Rg1对去卵巢大鼠面神经核脑源性神经营养因子表达的影响：半定量分析

BACKGROUND： Estrogen is neuroprotective effects such as breast carcinoma, endometria but long-term estrogen treatment can induce side cancer, and stroke. However, phytoestrogen is neuroprotective without these side effects. OBJECTIVE： To study the effects of Ginsenoside Rgl on facial neurons and brain-derived neurotrophic factor （BDNF） expression in the facial nucleus in ovariectomized rats. DESIGN, TIME AND SETTING： The randomized, controlled animal experiments were performed at the Ultrasonic Institute, Second Affiliated Hospital, Chongqing Medical University, China, from September 2007 to September 2008. MATERIALS： Ginsenoside Rgl （Sigma, USA）, rabbit anti-rat BDNF, Bcl-2, Bax antibodies, biotin-labeled goat anti-rabbit IgG （Boster, China）, and a TUNEL kit （Roche, Germany） were used in this study. METHODS： A total of 48 adult Sprague Dawley rats undergoing ovariectomy were randomly assigned into sham operation （n = 8）, model （n = 20）, and Ginsenoside Rgl （n = 20） groups. Facial nerve damage was induced by bilateral clamping of the facial nerve trunk. The bilateral facial nerve trunk was exposed in the sham operation group, with no clamping. Rats in the Ginsenoside Rgl group were intraperitoneally injected with 10 mg/kg per day Ginsenoside Rgl; other groups received 2 mL saline, once a day, for 14 days. MAIN OUTCOME MEASURES： Morphologic changes in neurons of the facial nucleus were observed following hematoxylin-eosin staining. Neuronal apoptosis was detected by TUNEL. Changes in ultrastructure of the facial nerve fibers were observed with a transmission electron microscope. Expression of BDNF, Bcl-2, and Bax protein was quantified by semiquantitative immunohistochemistry. RESULTS： At 3-14 days following facial nerve damage, Ginsenoside Rgl increased BDNF expression and the number of regenerated nerve fibers, and produced thicker myelin sheaths （P 〈 0.05）. Ginsenoside Rgl also gradually increased Bcl-2 protein expression and decreased Bax protein expression （P 〈 0.05）. By day 7, apoptosis was observed in facial neurons, but Ginsenoside Rgl reduced the number of apoptotic neurons. Sham animals did not show any changes in BDNF, Bcl-2, or Bax expression or facial neuron morphology. CONCLUSION： Ginsenoside Rgl can substantially inhibit facial neuronal apoptosis by increasing endogenous BDNF and Bcl-2 expression and by decreasing Bax expression in ovariectomized rats after facial nerve damage.     

经颅磁刺激对脑缺血大鼠皮层脑源性神经营养因子表达及梗死体积的影响

经颅磁刺激(transcranialmagneticstimulation,TMS)技术是近年来新开展的一项无痛无创的检测和治疗技术,治疗机制尚待商榷。我们对大鼠大脑中动脉阻塞/再灌注(middlecerebralarteryocclusion/reperfusion,MCAO/R)后经TMS干预,观察梗死灶周围皮层脑源性神经营养因子(brain deriv     

艾司西酞普兰对慢性应激大鼠海马脑源性神经营养因子基因外显子表达及DNA甲基化的影响

目的 探讨艾司西酞普兰对成年慢性应激大鼠海马脑源性神经营养因子(BDNF)基因不同外显子表达及DNA甲基化的影响.方法 以慢性不可预测温和应激(chronic unpredictablemild stress,CUMS)建立应激抑郁模型并予艾司西酞普兰干预.56只雄性Sprague-Dawley大鼠随机分为CUMS+水组、CUMS+药组、对照+水组及对照+药组,每组14只,以蔗糖水偏好试验评估大鼠抑郁样行为;模型建立第3周后分别检测上述各组大鼠海马BDNF基因第Ⅰ、Ⅱ、Ⅳ、Ⅵ外显子mRNA及BDNF总mRNA(第Ⅸ外显子)表达和第Ⅳ启动子区DNA甲基化水平.结果 (1)蔗糖水偏好试验:模型建立第2,3周,CUMS+水组[(34±21)％,(63±21)％]蔗糖水偏好均低于对照+水组[(67±15)％,(80±15)％],差异均有统计学意义(事后检验,P均＜0.05);而CUMS+药组[(58士19)％,(80±14)％]与对照+水组间的差异均无统计学意义(事后检验,P均＞0.05).(2)BDNF外显子表达:模型建立第3周,第Ⅳ外显子mRNA为BDNF总mRNA(第Ⅸ外显子)表达中的最主要者.CUMS+水组BDNF第Ⅳ及Ⅸ外显子mRNA水平[(4.64±0.65)×10-3,(5.73±0.79) ×10-3]均低于对照+水组[ (6.14±0.87)×10-3,(6.82±0.35)×10-3],差异均有统计学意义(事后检验,P均＜0.05);而CUMS+药组[(5.69±0.18)×10-3,(6.91±0.98)×10-3]与对照+水组间的差异均无统计学意义(事后检验,P均＞0.05).(3)DNA甲基化:各组大鼠海马BDNF第Ⅳ启动子区DNA均未发生甲基化.结论 艾司西酞普兰主要调节BDNF第Ⅳ外显子转录阻止CUMS成年大鼠海马的该基因表达下降,艾司西酞普兰第Ⅳ启动子区DNA甲基化无影响.     

Downhill training upregulates mice hippocampal and striatal brain-derived neurotrophic factor levels

This study examined the effects of downhill treadmill exercise on brain-derived neurotrophic factor (BDNF) protein on the hippocampus and striatum of mice. Twenty-four adult mice were assigned to three groups: non-runners control, level or downhill (16 degrees decline) running exercise. The exercise schedule consisted of progressive treadmill running for 5 days week(-1) over 8 weeks. Blood lactate levels classified exercise intensity as moderate to high. Both training types increased citrate synthase activity of the soleus muscle when compared to untrained controls. While level running increased BDNF levels selectively in the hippocampus (68.5%), the eccentric running resulted in a pronounced BDNF increase in both the hippocampus (137.0%) and the striatum (49.9%). Further studies will specify whether the observed alterations in BDNF are due to downhill-induced upregulation or complex learning-induced mechanisms that influence BDNF levels in these brain regions.     

姜黄素对肠易激综合征模型大鼠5-羟色胺和脑源性神经营养因子的影响

目的 从脑肠轴角度明确肠易激综合征(IBS)发病机制,观察姜黄素对IBS的疗效.方法 48只SD大鼠按随机数字表法分为6组:正常组,IBS模型组,姜低组、姜中组、姜高组(造模前分别灌胃给予姜黄素10、20、40 mg/kg),丙咪嗪组(造模前腹腔注射丙咪嗪10 mg/kg),每组各8只.采用大鼠慢急性联合应激模型模拟IBS.糖水消耗试验和内脏敏感性实验检测各组大鼠抑郁样行为和肠道敏感性,高效液相法及Western blotting分别测定大鼠大脑皮层和回肠5-羟色胺(5-HT)及脑源性神经营养因子(BDNF)的表达. 结果 IBS模型组大鼠糖水消耗量明显减少,肠道内脏敏感性明显升高,大脑额叶皮层5-HT、BDNF表达水平降低,回肠黏膜5-HT、BDNF表达水平明显升高,与正常组比较差异均有统计学意义(P＜0.05).给予不同剂量姜黄素后能逆转上述行为学改变及大脑皮层、回肠的5-HT 、BDNF水平变化,其中姜高组与IBS模型组比较差异均有统计学意义(P＜0.05).丙咪嗪组效果与姜高组类似. 结论 IBS大鼠脑肠内5-HT、BDNF表达异常说明IBS的发生存在脑肠改变的物质基础.姜黄素可能是通过调节5-HT、BDNF表达来改善IBS模型大鼠的行为学变化.     

驽药针刺对大鼠脊髓损伤后运动功能及BDNF表达的影响

目的研究驽药针刺在大鼠脊髓损伤后运动功能变化以及BDNF表达的变化。方法采用脊髓半横断损伤模型。100只SD大鼠随机分为对照组、假手术组、脊髓损伤组、单纯针刺组、驽药针刺组,每组分为3天、7天、14天、21天共4个亚组,每组5只。BBB法评定大鼠后肢运动功能变化,免疫组化法检测大鼠脊髓中BDNF的表达变化。结果 BBB评分显示驽药针刺组的各时间点评分均高于脊髓损伤组(P0.05),驽药针刺组7、14、21d的BDNF表达均高于脊髓损伤组(P0.05),且与BBB评分呈正相关(r=0.717,P0.05)。结论驽药针刺可明显改善脊髓损伤大鼠的运动功能,并可明显促进大鼠脊髓损伤后BDNF的表达。     

侧脑室内注入脑源性神经营养因子对AD小鼠酪氨酸激酶B及内源性BDNF表达的影响

目的 探讨侧脑室内注入脑源性神经营养因子(BDNF)对APP/PS1双转基因阿尔茨海默病(AD)小鼠酪氨酸激酶B (TrkB)及内源性BDNF表达的影响. 方法 10只10月龄APP/PS1雄性小鼠按随机数字表法分为2组,实验组5只,双侧侧脑室内注入BDNF;磷酸盐缓冲液(PBS)组5只,双侧侧脑室内注入PBS,为阳性对照组;干预时间均为6周.同时选择5只同窝生10月龄野生型小鼠,不予任何处理,为阴性对照组.采用荧光免疫组化法观察小鼠皮层区β-淀粉样蛋白(Aβ)斑块形态学改变,硫磺素S法检测致密斑的数量,同时检测小鼠皮层区TrkB、BDNF蛋白表达的情况. 结果 (1)治疗前、后BDNF组Aβ斑块总数分别为(101.58±7.86)个、(102.83±8.22)个,与PBS组(97.23±1 1.62)个、(103.6±6.46)个比较差异均无统计学意义(t=0.695、-0.171,P=-0.509、0.869);治疗6周后BDNF组Aβ斑块直径缩小至(34.65±9.33)μm,TS+斑块数量减少至(51.70±4.18)个,与PBS组(46.17±10.16)μm、(58.85±7.55)个比较,差异均具有统计学意义(t=-2.401、-2.536,P=0.047、0.039);(2)治疗后BDNF组TrkB、BDNF蛋白表达明显增强. 结论 侧脑室内注入BDNF减少了Aβ致密斑的形成,使Aβ蛋白沉积导致的神经毒性作用减弱,从而促进皮层区TrkB表达增强,导致内源性BDNF表达增强,可在一定程度上延缓AD小鼠的病程.     

精神分裂症患者脑源性神经营养因子水平及其与临床症状的关系

目的探讨脑源性神经营养因子（BDNF）在精神分裂症病理生理机制中的可能作用。方法采用横断面病例一对照研究设计。患者组为48例精神分裂症患者，其中发病后从未治疗组31例，停止治疗组17例。正常对照组（以下简称对照组）为与患者组性别、年龄匹配的41名健康人。对患者组用阳性和阴性症状量表（PANSS）评定病情严重程度。血浆BDNF浓度用酶联免疫吸附试验测定。用多变量方差分析比较组间差异。结果从未治疗组[（4．5±2．2）μg/L]和停药组患者[（3．9±1．4）μg/L]血浆BDNF浓度均低于对照组[（6．5±2．2）μg/L]（F检验，P〈0．01）；而从未治疗组与停止治疗组的差异无统计学意义（P〉0．05）。患者组的血浆BDNF浓度与PANSS阴性症状因子分（r=-0．509；P〈0．01）及总病期呈负相关（r=-0．426；P〈0．01），与发病年龄、PANSS阳性因子分、总分的相关性均无统计学差异。结论精神分裂症患者BDNF浓度低于正常；BDNF可能是参与精神分裂症病理生理机制的一种重要物质。     

睫状神经营养因子对抑郁大鼠行为和海马神经元损伤的影响

目的　观察中枢给予外源性睫状神经营养因子 (CNTF)对抑郁大鼠行为和海马神经元损伤的影响。方法　将 60只SD雄性大鼠随机分为正常对照组 (NC组 )、生理盐水 +抑郁组 (S +D组 )、CNTF 3 0 0 0U +抑郁组 (Ch+D组 )和CNTF 30 0U +抑郁组 (Cl+D组 ) ,每组 1 5只。采用长期不可预见性中等强度应激造成大鼠抑郁模型 ,于实验开始前 1天和实验第 7,1 4 ,2 2天用Openfield法测定大鼠行为 ,于应激第 2 2天将其处死 ,固定脑组织 ,用组织化学、光镜和电镜等技术观察海马CA1、CA3及齿状回神经元的数目和形态。结果　 (1 )应激第 2 2天 ,S +D组体重增长的g数 [(2 8 2 2± 4 2 2 )g]和蔗糖溶液消耗量 [(7 33± 2 43)g]均低于NC组 [分别为 (1 2 4 95± 6 44)g和 (2 0 50± 4 80 )g;P <0 0 1 ] ;而Ch+D组 [分别为 (64 72± 1 5 69)g和 (1 5 56± 3 48)g]均高于S +D组 (P <0 0 1 )。 (2 )Ch+D组的抑郁行为 [水平运动为 (9 80± 1 2 3)次 / 3min ,垂直运动中位数为 3次 / 3min]较S +D组 [水平运动为(1 1 6± 0 41 )次 / 3min ,垂直运动中位数为 0次 / 3min]有显著改善 (P <0 0 1 )。 (3)S +D组和Cl+D组各脑区神经元的丢失均多于NC组 (P <0 0 5和P <0 0 1 ) ,而Ch+D组神经元的丢失则少于S +D组和Cl+D组 (P <0 0     

Release of immunoreactive brain-derived neurotrophic factor in the spinal cord of the rat following sciatic nerve transection

Using the antibody microprobe method, the sites of spinal release of immunoreactive brain-derived neurotrophic factor (BDNF) was studied in normal rats, and rats with prior sciatic nerve transection. In normal rats, a significant basal release of immunoreactive BDNF was found in the superficial dorsal horn. Following sciatic nerve transection (performed 14 days previously), release of BDNF was found throughout the whole of the dorsal horn, extending into deeper laminae. Electrical stimulation of the ipsilateral sciatic nerve at a strength adequate to excite either A fibres (20 Hz at 2x threshold voltage) or A and C fibres (2 Hz at 20x threshold voltage) did not alter the basal release of immunoreactive BDNF in normal or in nerve-injured rats. The results suggest that BDNF is released from the central terminals of primary afferent fibres, but such release is not solely dependent upon action potential invasion of these terminals. The increased extent of release following nerve transection is consistent with the hypothesis that BDNF plays a role in the central response to peripheral nerve injury.     

Serum concentrations of brain-derived neurotrophic factor in patients with gender identity disorder

Gender Identity Disorder (GID) is characterized by a strong and persistent cross-gender identification that affects different aspects of behavior. Brain-derived neurotrophic factor (BDNF) plays a critical role in neurodevelopment and neuroplasticity. Altered BDNF-signaling is thought to contribute to the pathogenesis of psychiatric disordersand is related to traumatic life events. To examine serum BDNF levels, we compared one group of DSM-IV GID patients (n = 45) and one healthy control group (n = 66). Serum BDNF levels were significantly decreased in GID patients (p = 0.013). This data support the hypothesis that the reduction found in serum BDNF levels in GID patients may be related to the psychological abuse that transsexuals are exposed during their life.     

Low serum levels of brain-derived neurotrophic factor and epidermal growth factor in patients with chronic schizophrenia

Neurotrophic factors (NFs) play a pivotal role in the development of the central nervous system. They are thus also suspected of being involved in the etiology of schizophrenia. Previous studies reported a decreased level of serum brain-derived neurotrophic factor (BDNF) in schizophrenia, whereas the association of epidermal growth factor (EGF) with this illness remains controversial. Using a two-site enzyme immunoassay, we conducted the simultaneous measurement of serum BDNF and EGF levels in a group of patients with chronic schizophrenia (N = 74) and a group of normal controls matched in age, body mass index, smoking habit and sex (N = 87). We found that, compared to normal controls, patients with chronic schizophrenia exhibited lower serum levels of both BDNF and EGF across all ages examined (21–59 years). The serum levels of BDNF and EGF were negatively correlated in the controls (r = − 0.387, P = 0.0002) but not in the patients. Clinical parameters such as duration of illness and psychiatric rating scale also showed no robust correlations with the NF levels. Collectively, these results suggest that pervasive, abnormal signaling of NFs underlies the pathophysiology of chronic schizophrenia.     

学习障碍患儿血清BDNF水平的研究

目的探讨学习障碍血清脑源性神经营养因子(BDNF)水平的变化,及其与学习障碍病理基础的关系。方法患者组为22例未治疗过且不共患其他疾病的学习障碍患儿,对照组为16例年龄性别匹配正常儿童,以瑞文标准推理测验(SPM)测定智商,BDNF采用酶联夹心免疫吸附法检测。结果LD患者血清BDNF浓度为:平均(4.603±3.620)ng/ml高于对照组(1.843±0.728)ng/ml(t=3.326,P=0.003<0.01)。边缘智商组(4.523±4.618)ng/ml,与正常对照组比较差异有非常显著性(P=0.008<0.01)。结论学习障碍患儿血清BDNF浓度高于正常儿童,边缘智商者升高更明显。