抗抑郁剂对慢性应激抑郁大鼠脑内β肾上腺素受体作用机制研究

目的观察慢性应激抑郁大鼠大脑额叶皮层总β肾上腺素受体及亚型功能改变,研究抗抑郁剂阿米替林、氟西汀、帕罗西汀对中枢β肾上腺素受体的影响。探讨抑郁症发病机制及抗抑郁剂治疗的中枢作用机制。方法采用放射性配体受体分析法,测定慢性应激抑郁大鼠大脑额叶皮层总β肾上腺素受体及β肾上腺素受体亚型功能改变;并测定抗抑郁剂阿米替林、氟西汀、帕罗西汀对皮层总β肾上腺素受体及β肾上腺素受体亚型功能的影响。结果抑郁大鼠额叶皮层总β受体、β1受体明显上调,阿米替林、氟西汀、帕罗西汀长期治疗均可明显下调额叶皮层β受体及β1受体发挥抗抑郁作用。结论慢性应激抑郁大鼠大脑额叶皮层β受体明显上调是由于β1受体亚型上调所致。长期应用抗抑郁剂阿米替林、氟西汀、帕罗西汀治疗可能是通过下调β受体主要是β1受体亚型而发挥抗抑郁作用。     

电针对慢性应激抑制模型大鼠脑单胺类神经递质的影响

目的 探讨电针刺百会，印堂穴对慢性应激抑郁模型大鼠脑内单胺类神经递质的影响及治疗抑郁症的机理。方法 将２４只Ｓｐｒａｇｕｅ－Ｄａｗｌｅｙ雄性大鼠随机分为对照组，抑郁模型组，抑制模型电针组和抑郁模型加阿米替林组，每组６只，用高效液相－电化学法测定大鼠脑内单胺类神经递质及其代谢产物的含量，比较含量的比值。结果 抑郁模型组大鼠脑皮层５－羟色胺（５－ＨＴ）／５－羟吲哚乙酸（５－ＨＩＡＡ），纹状体多巴胺（Ｄ     

电针与阿米替林治疗抑郁状态对照观察

我们用电针治疗抑郁状态患者,以阿米替林为对照进行观察,报告如下。1对象和方法为1994至1995年北京大学第六医院和我院门诊及住院患者,符合中国精神疾病分类方案与诊断标准第2版修订本的抑郁症、抑郁性神经症、心因性精神障碍(抑郁)或器质性精神障碍(抑郁)的诊断标准,Hamilton抑郁量表(HAMD)评分>20分。共47例,其中电针组27例,男15例,女12例;平均年龄37·8岁;平均病程8·8个月。阿米替林组20例,男11例,女9例;平均年龄35·9岁;平均病程6·8个月。两组以上各项差异均无显著性(P均>0·05)。电针取百会、印堂穴,斜刺1寸,用G6850型电针治疗仪,…     

慢性应激抑郁模型大鼠强迫游泳后海马中HsP70的表达

目的研究慢性应激对强迫游泳大鼠海马神经元热休克蛋白70(Hsp70)表达的影响。方法将50 只大鼠随机分为实验组和对照组各25只。实验组大鼠通过21天的应激刺激制作抑郁动物模型,此期间对照组大 鼠正常饲养。此后所有大鼠逐只进行急性强迫应激刺激。采用特异性抗体的免疫组织化学方法,观察2组大鼠在 强迫游泳后2 h、6 h、18 h、24 h和48 h各时点海马神经元Hsp70的表达情况。结果慢性应激抑郁大鼠模型接受 急性强迫游泳应激后,海马CA3区和齿状回(DG)内Hsp70蛋白的表达较对照组强迫游泳后显著降低(P<0．05)。 结论慢性应激使大鼠在急性强迫游泳应激后海马CA3区和DG内Hsp70的表达降低。     

电针对慢性应激抑郁模型大鼠脑单胺类神经递质的影响

目的　探讨电针刺激百会、印堂穴对慢性应激抑郁模型大鼠脑内单胺类神经递质的影响及治疗抑郁症的机理。方法　将２４ 只ＳｐｒａｇｕｅＤａｗｌｅｙ 雄性大鼠随机分为对照组、抑郁模型组、抑郁模型加电针组和抑郁模型加阿米替林组,每组６ 只。用高效液相电化学法测定大鼠脑内单胺类神经递质及其代谢产物的含量,比较含量的比值。结果　抑郁模型组大鼠脑皮层５羟色胺（５ＨＴ）／５羟吲哚乙酸（５ＨＩＡＡ） 、纹状体多巴胺（ＤＡ）／３,４二羟基苯乙酸（ＤＯＰＡＣ） 分别为０－５０ ±０－１７,１０－３７ ±１－４０,低于对照组（ 分别为０－８８±０－２５ ,１２－３６ ±１－５０）,Ｐ＜ ０－０５ ;皮层去甲肾上腺素（ＮＥ）／５ＨＴ（２－８８ ±１－００） 高于对照组（１－７３±０－４０） ,Ｐ＜ ０－０５。电针刺激百会、印堂穴可使模型大鼠脑皮层５ＨＴ／５ＨＩＡＡ 与ＮＥ／５ＨＴ恢复正常（Ｐ＜０－０５） ,对纹状体ＤＡ／ＤＯＰＡＣ 的降低无影响（ Ｐ＞ ０－０５）。结论　提示电针刺激百会、印堂穴通过降低皮层５ＨＴ的代谢,提高５ＨＴ能神经的活性,并协调ＮＥ 与５ＨＴ之间的平衡来发挥抗抑郁作用。     

重复经颅磁刺激对抑郁模型大鼠行为学及海马区糖皮质激素受体表达的影响

目的观察重复经颅磁刺激(repetitive transcranial magnetic stimulation,r TMS)对慢性应激抑郁模型大鼠的抗抑郁作用及对海马区糖皮质激素受体(glucocorticoid receptor,GR)表达的影响,探讨r TMS抗抑郁作用的可能机制。方法 75只健康成年雄性大鼠随机分为造模组(60只)和空白对照组(15只),造模组采用孤养联合慢性温和不可预见应激(chronic unpredictability stimulus,CUMS)方法制备抑郁大鼠模型,为期3周,筛选造模成功的大鼠45只随机分为r TMS组、伪r TMS组和抑郁对照组,每组15只,r TMS组和伪r TMS组分别接受10 Hz的r TMS刺激和伪刺激干预3周,抑郁对照组和空白对照组不给予干预。分别于造模前、造模后、r TMS干预后进行体重测量、蔗糖水消耗实验和强迫游泳实验评估,r TMS干预后检测大鼠海马区GR蛋白和海马GR m RNA表达水平。结果造模后,r TMS组、伪r TMS组和抑郁对照组大鼠蔗糖水消耗量较空白对照组下降,强迫游泳不动时间增加(P0.01)。r TMS干预后,r TMS组体重增长率、蔗糖水消耗量与伪r TMS组和抑郁对照组相比均较高(P0.01),强迫游泳不动时间较短(P0.01)。伪r TMS组及抑郁对照组海马区GR蛋白及其m RNA表达水平与r TMS组和空白对照组相比均较低(P0.05)。结论 r TMS能够改善CUMS抑郁模型大鼠的抑郁样行为,可能与上调海马区GR表达有关。     

慢性利血平抑郁模型大鼠脑内游离钙离子、钙调素和环核苷酸含量的变化

为探讨利血平致抑郁及阿米替林抗抑郁的机理，将Ｗｉｓｔａｒ雄性大鼠随机分为对照组、利血平模型组和利血平加阿米替林组，测定了大鼠脑内游离钙离子、钙调素、环核苷酸含量变化。结果显示，模型大鼠脑内游离钙离子、钙调素和环核苷酸含量降低，阿米替林可使模型大鼠脑内游离钙离子、钙调素浓度升高，而对环核苷酸则无影响。提示利血平致抑郁的机理与２条第二信使通路均有关，而阿米替林则可能是通过作用于钙信号系统发挥其抗抑郁作用。     

抑郁模型大鼠中枢G蛋白的研究

目的 探讨抑郁模型人鼠中枢部分脑区Gαi蛋白的表达水平及其与部分抗抑郁剂作用机制的关系.方法 50只大鼠随机分为氨米帕明组、两酞普兰组、联合(碳酸锂加西酞普兰)干预组、生理盐水组、空白对照组,前4组接受慢件非顶见性应激制备为抑郁模型大鼠,并分别给予相应的干预措施;以强迫游泳试验评价药物疗效,利用免疫组织化学方法检测大鼠前额皮质、海马CA3、纹状体Gαi蛋白的表达.结果 实施干预4周后各组大鼠强迫游泳不动时间明硅延长,与末接受应激的空白对照组比较差异有统计学意义(F=2.61,P＜0.05),联合干预组强迫游泳不动时间于用药第1周恢复正常(F=4.58,P＜0.05),西肤普兰组于第2周恢复止常(F=4.33,P＜0.05),氯米帕明组于第3周恢复正常(F=2.86,P＜0.05);干预结束后,生理盐水组前额皮质、海马CA3区Gαi灰度值明显较空白对照组减少(F=2.75,P＜0.05;F=2.71,P＜0.05),药物干预后各组与空白对照组则无明显差异(P＞0.05);干预结束时,各组大鼠第4次强迫游泳小动时间和各脑区Gαi灰度值没有相关性(r=-0.28～0.495,P均大于O.05).结论 抑郁模型大鼠前额皮质、海马CA3 Gαi表达升高,恢复前额皮质、海马CA3的Gαi的表达可能是抗抑郁剂的作用靶点之一.     

文拉法辛对慢性应激抑郁大鼠海马区可塑性相关蛋白mRNA表达的影响

目的 观察文拉法辛对慢性应激抑郁大鼠海马区可塑性相关蛋白mRNA表达的影响.方法 用慢性不可预见应激(CUS)方法建立大鼠抑郁模型,给予2种剂量(5 mg/kg体质量和10 mg/kg体质量)的抗抑郁剂文拉法辛,用反转录-聚合酶链反应检测大鼠海马区脑源性神经营养因子(BDNF)、转录因子环磷腺苷反应元件结合蛋白(CREB)及神经细胞黏附分子(NCAM)mRNA表达的变化.正常对照组、抑郁模型组、抑郁模型后注射生理盐水14 d组及28 d组各10只,抑郁模型后小剂量文拉法辛(5 mg/kg体质量)治疗14 d组及28 d组、抑郁模型后大剂量文拉法辛(10 mg/kg体质量)治疗14 d组及28 d组各11只.结果 抑郁模型大鼠体质量、蔗糖水消耗量及旷场实验结果均明显低于正常对照组,提示抑郁模型大鼠在第28天建立成功.慢性不可预见应激28 d后,抑郁模型大鼠海马区BDNF(0.18±0.09)、CREB(0.10±0.05)及NCAM(0.08±0.04)mRNA表达水平均明显低于正常组[吸光度比值分别为(0.41±0.12)、(0.26±0.05)及(0.24±0.08);P均＜0.05 ].5 mg/kg体质量文拉法辛明显增加海马区3种可塑性相关蛋白mRNA的表达;10 mg/kg文拉法辛轻度降低海马区3种可塑性相关蛋白mRNA的表达.结论 文拉法辛在一定剂量范围内调节海马区的神经可塑性,BDNF、CREB及NCAM在抑郁症的病因及治疗中发挥重要作用.     

无抽搐电休克治疗大鼠抑郁症的谷氨酸能机制研究

目的 观察抑郁大鼠电休克治疗后海马内谷氨酸含量以及N-甲基-D天门冬氨酸(NMDA)受体的表达,探讨电休克治疗抑郁症的谷氨酸能神经机制.方法 36只SD大鼠随机分为无抽搐电休克组(电休克组)、抑郁模型对照组(抑郁组)、对照组,每组12只.前两组采用孤养加慢性不可预见性应激建立抑郁模型,建模后电休克组在丙泊酚麻醉下行无抽搐电休克治疗,隔天1次共2周.检测各组海马谷氰酸含量和海马CA1区、CA3区NMDA受体2B亚单位(NMDA-NR2B)的表达.结果 ①电休克治疗后电休克组大鼠水平移动格数、垂直竖立次数和糖水消耗量都高于抑郁组(P＜0.01).②电休克组大鼠海马内谷氨酸含量低于抑郁组(P＜0.01),而抑郁组高于正常组(P＜0.01).③电休克组大鼠海马CA1区和CA3区NMDA-NR2B的表达量高于正常组(P＜0.05),而抑郁组低于正常组(P＜0.01).结论 无抽搐电休克治疗可抑制抑郁症模型大鼠海马内谷氨酸含量的升高并使NMDA-NR2B的表达量上调,这可能足其抗抑郁机制之一.     

The effect of age of onset of PD on risk of dementia

Background Dementia occurs in the majority of patients with Parkinson’s disease (PD). Late onset of PD has been reported to be associated with a higher risk for dementia. However, age at onset (AAO) and age at baseline assessment are often correlated. The aim of this study was to explore whether AAO of PD symptoms is a risk factor for dementia independent of the general effect of age. Methods Two community-based studies of PD in New York (n = 281) and Rogaland county, Norway (n = 227) and two population-based groups of healthy elderly from New York (n = 180) and Odense, Denmark (n = 2414) were followed prospectively for 3–4 years and assessed for dementia according to DSM-IIIR. All PD and control cases underwent neurological examination and were followed with neurological and neuropsychological assessments. We used Cox proportional hazards regression based on three different time scales to explore the effect of AAO of PD on risk of dementia, adjusting for age at baseline and other demographic and clinical variables. Findings In both PD groups and in the pooled analyses, there was a significant effect of age at baseline assessment on the time to develop dementia, but there was no effect of AAO independent of age itself. Consistent with these results, there was no increased relative effect of age on the time to develop dementia in PD cases compared with controls. Interpretation This study shows that it is the general effect of age, rather than AAO that is associated with incident dementia in subjects with PD. Received in revised form: 22 December 2005     

腺垂体功能减退症临床特征变化分析

目的探讨腺垂体功能减退症患者的病因结构变化及临床表现。方法回顾性分析我院2013-01—2016-12住院及门诊78例腺垂体功能减退症患者的临床资料。结果男32例(41.03%),女46例(58.97%);诊断时年龄11~89岁,平均62.5岁;鞍区占位(包括术前及术后)52例(66.67%),席汉综合征8例(10.26%),空泡蝶鞍9例(11.65%),病因不明8例(10.26%),垂体-下丘脑发育不良1例(1.28%)。首次就诊科室:纳差厌食、恶心呕吐就诊于消化内科36例(46.15%)最常见。ACTH+TSH+Gn+G激素缺乏为19例最多,占24.36%,ACTH+TSH+Gn缺乏15例,占19.23%。结论腺垂体功能减退症病因结构发生变化,发病人群、首发症状及受累激素也不同,患者女性多于男性,发病年龄偏高,症状不典型,分布于临床多个科室,其中以低钠血症为首发临床表现就诊消化内科最多。     

Standards of instrumentation of EMG

Standardization of Electromyography (EMG) instrumentation is of particular importance to ensure high quality recordings. This consensus report on “Standards of Instrumentation of EMG” is an update and extension of the earlier IFCN Guidelines published in 1999. First, a panel of experts in different fields from different geographical distributions was invited to submit a section on their particular interest and expertise. Then, the merged document was circulated for comments and edits until a consensus emerged.The first sections in this document cover technical aspects such as instrumentation, EMG hardware and software including amplifiers and filters, digital signal analysis and instrumentation settings. Other sections cover the topics such as temporary storage, trigger and delay line, averaging, electrode types, stimulation techniques for optimal and standardised EMG examinations, and the artefacts electromyographers may face and safety rules they should follow. Finally, storage of data and databases, report generators and external communication are summarized.     

帕金森病运动症状进展分析

目的分析帕金森病(PD)患者运动症状进展特点。方法采用PD统一评分量表(UPDRS)Ⅲ对912例PD患者进行评估。结果与病程1年的患者比较,除病程1~2年的患者外,其他病程患者的UPDRSⅢ评分、强直分、姿势或步态异常分、轴性症状总分、言语分、步态分显著升高(均P0.05),病程5~6年及14年患者的震颤分,病程5~6年、7~8年、9~13年、14年患者的运动迟缓分、姿势分显著升高(P0.05~0.01)。轴性症状进展速度高于UPDRSⅢ评分。结论 PD患者病程早期UPDRSⅢ评分进展快,震颤症状进展独立于其他症状,轴性症状评分较UPDRSⅢ更敏感地反映疾病加重趋势。     

Frequency of accumulation of filaments in adaxonal cytoplasm of Schwann cells of myelinated fibers of rat spinal roots

Summary The frequency of accumulation of 6-nm filaments in the adaxonal cytoplasm of Schwann cells in the 6th lumbar dorsal and ventral roots was evaluated in 4-, 8-, 26- and 45-week-old Sprague-Dawley rats. The frequency was higher in 4- and 8-week-old (growing) rats than in 26- and 45-week old (mature) rats, and also higher in ventral than in dorsal roots in 4-, 8- and 26-week old rats. There were no clusters on certain groups of myelinated fibers according to the size of transverse axonal area, in both the ventral and dorsal roots. Therefore, this accumulation may reflect certain functions of the adaxonal cytoplasm of Schwann cell during natural growth and maturation of the axon and myelin sheath.     

Function of circle of Willis

Nearly 400 years ago, Thomas Willis described the arterial ring at the base of the brain (the circle of Willis, CW) and recognized it as a compensatory system in the case of arterial occlusion. This theory is still accepted. We present several arguments that via negativa should discard the compensatory theory. (1) Current theory is anthropocentric; it ignores other species and their analog structures. (2) Arterial pathologies are diseases of old age, appearing after gene propagation. (3) According to the current theory, evolution has foresight. (4) Its commonness among animals indicates that it is probably a convergent evolutionary structure. (5) It was observed that communicating arteries are too small for effective blood flow, and (6) missing or hypoplastic in the majority of the population. We infer that CW, under physiologic conditions, serves as a passive pressure dissipating system; without considerable blood flow, pressure is transferred from the high to low pressure end, the latter being another arterial component of CW. Pressure gradient exists because pulse wave and blood flow arrive into the skull through different cerebral arteries asynchronously, due to arterial tree asymmetry. Therefore, CW and its communicating arteries protect cerebral artery and blood–brain barrier from hemodynamic stress.     

Effects of prevention of afferentation of the development of the chick optic lobe

BONDY, S. C., M. E. HARRINGTON AND C. L. ANDERSON. Effects of prevention of afferentation on the developmentof the chick optic lobe. BRAIN RES. BULL. 3(5) 411–413, 1978.—The effects of unilateral extirpation of the right optic cup of the three-day incubated chick embryo upon the rate of synthesis and the stability of DNA in the non-innervated optic lobe, have been studied. This surgical procedure prevents innervation of the optic lobe contralateral to the removed eye, while the other optic lobe is normally innervated by retinal ganglion cells of the remaining eye. At the 20th day of incubation, the DNA content of the non-innervated lobe was below that of the paired lobe receiving normal innervation. This deficiency of cell number was caused by two events; death of an excess number of neurons formed early in embryogenesis and a reduced rate of glial proliferation in the later stages of incubation.     

Release of endogenous catecholamines from slices of hypothalamus of rats

The release of endogenous catecholamines from superfused slices of rat hypothalamus was studied under basal conditions and during release evoked by 40 mM K⁺. Catecholamines in superfusates, and in extracts of the tissue after stimulation, were isolated by column chromatography and quantitated by liquid chromatography with electrochemical detection. Norepinephrine (NE) was not consistently demonstrable in superfusate collected under basal conditions, but 40 mM K⁺ caused the release of from 2 to 4 ng/g of tissue per min. The addition of cocaine to the superfusate caused increases in basal and evoked release of NE. Epinephrine (E) could be measured in superfusates of slices from male but not female rats and then only when cocaine was added to the superfusate. Accordingly, the concentration of E in hypothalamus was greater in male rats than in female rats. Dopamine (DA) was not consistently measurable in the spontaneous overflow from slices either in the presence or absence of cocaine. K⁺-evoked release of DA could be demonstrated in slices from female rats. The addition of cocaine increased the evoked release of DA from slices from both sexes. Corticosterone, added to cocaine, had no effects on the efflux of any of the catecholamines. The experiments suggest that neuronal reuptake of all catecholamines is very efficient in the hypothalamus both under basal conditions and during evoked release.     

《绵阳市社会心理服务工作管理办法》解读

2018年,国家卫生健康委员会等10部委联合发布《关于印发全国社会心理服务体系建设试点工作方案的通知》,四川省绵阳市被列为全国第一批试点地区。绵阳市人民政府依据《中华人民共和国精神卫生法》等相关法律法规和文件精神,结合前期调查研究和社会心理服务工作的试点实际,编制出台了《绵阳市社会心理服务工作管理办法》,并于2021年12月25日起施行。本文围绕社会心理服务的相关概念、办法总则、重点内容、保障措施等方面进行解读,以期为社会心理服务工作的规范、持续和有效开展提供参考。     

阿立哌唑对精神分裂症患者生活质量的影响

目的:比较阿立哌唑与利培酮对精神分裂症患者生活质量的影响。方法:60例精神分裂患者随机平分为两组各30例,分别给予阿立哌唑和利培酮治疗。疗程8周。用生活质量综合评定问卷-74(GQOLI-74)、阳性与阴性症状量表(PANSS)及副反应量表(TESS)评定疗效及不良反应。结果:阿立哌唑与利培酮均能显著提高精神分裂症患者生活质量,但阿立哌唑在改善GQOLI-74总分、躯体健康及社会功能维度优于利培酮。结论:阿立哌唑治疗有利于提高精神分裂症患者生活质量。