Effects of selective NMDA and non-NMDA blockade in the nucleus accumbens on the plus-maze test

Effect of blocking N-methyl-D-aspartic acid (NMDA) and non-NMDA-glutamatergic receptors on performance in the plus-maze was studied in male rats bilaterally cannulated into the nucleus accumbens (Acc). Rats were divided into seven groups that received either 1 microl injections of saline, (+/-)2-amino-7-phosphonoheptanoic acid (AP-7, 0.2, 0.5, or 1 microg) or 2,3 dioxo-6-nitro-1,2,3,4,tetrahydrobenzo-(f)quinoxaline-7-sulphonamide disodium (NBQX, 0.2, 0.5, or 1 microg) 15 min before testing. Time spent in open arm, time per entry, end arrivals, open, closed, and total arm entries, relationship between open-, closed-, and total arm entries, rearing, face-, head-, and body grooming, and number of fecal boli were recorded. Time spent in the open arm increased under AP-7 (0.5 and 1 microg; P<.01) and NBQX (1 microg; P<.05) treatment, whereas time per entry was increased only with AP-7 (1 microg; P<.05). Open arm entries were increased by the intermediate doses of AP-7 (0.5 microg; P<.01) and NBQX (0.5 microg; P<.05); end arrivals were increased by the intermediate dose of AP-7 (0.5 microg/1 microl, P<.05). The frequency of rearing, grooming, and closed arm entries was not affected by the treatment. We conclude that NMDA and non-NMDA-glutamatergic blockade in the Acc lead to a behavioral disinhibition of cortical influences with the median doses, but that at higher doses the blockers have an anxiolytic-like effect.     

Enhancement of attention in man with ACTH/MSH 4–10

Normal men were infused for 4 hr with ACTH/MSH 4–10 or a control solution. Behavioral testing after the infusion indicated that subjects who received ACTH/MSH 4–10 were less anxious and had better visual memory than control subjects but the predominant effect of the heptapeptide was to increase visual attention. It was specualted that ACTH/MSH 4–10 may be uniquely coded for attentional functioning.     

重点理工科高校大一新生焦虑状况及相关因素的研究

目的探讨重点理工科学校大一新生焦虑状况及相关因素,为进行针对性的干预提供依据。方法以广东某重点理工高校2007级的大一学生为研究对象,采用自行设计一般项目调查表、状态-特质焦虑量表（STAI）、匹兹堡睡眠质量指数量表（PSQI）、应付方式问卷进行测评。结果测查学生不论男女状态焦虑、特质焦虑分均显著高于地方常模;19.29%的学生睡眠质量较差;高状态焦虑组和高特质焦虑组解决问题、求助应付因子分均显著低于低状态焦虑组和低特质焦虑组,而自责、幻想、退避应付因子分则显著高于低状态焦虑组和低特质焦虑组;多元逐步回归分析说明,学生如常采用解决问题应付方式,在一定程度上可避免焦虑的产生,而睡眠质量差、采用自责应对方式则可加重焦虑水平。结论采取有效的认知应对策略其意义是使学生改变应激源,以使其变得威胁较小或变成挑战,把情绪基调训练成兴奋、期待和征服。     

糖尿病患者心理健康状况的多因素Logistic回归分析

目的探讨糖尿病患者心理健康状况的影响因素。方法对山西省4个地区8个调查点的2132名城乡居民，其中包括139名糖尿病患者，进行问卷调查，了解其一般情况以及情绪状况、社会支持等社会心理因素。结果单因素分析发现，糖尿病患者的焦虑情绪高于非糖尿病者，对社会支持中的家庭资源的利用也不及非糖尿病者；多因素发现，影响糖尿病患者心理健康状况的因素有地区、性别、年龄、经济收入、焦虑以及抑郁等；结论糖尿病患者心理健康状况的影响因素既涉及地区、性别、年龄、经济收入等一般状况，也与患者的情绪障碍的社会支持有密切关系。临床应根据不同的影响因素进行有效牙心理干预。     

Association between variation in the vesicular monoamine transporter 1 gene on chromosome 8p and anxiety-related personality traits

Vesicular monoamine transporters are involved in the presynaptic packaging of norepinephrine, dopamine and serotonin into storage vesicles. The vesicles release their content upon arrival of an action potential into the synaptic cleft. Dysregulation of monoaminergic neurotransmission has been long postulated to play a relevant role in the etiology of neuropsychiatric disorders. The gene encoding the vesicular monoamine transporter 1 (VMAT1/SLC18A1) maps to chromosome 8p21, a region where several linkage peaks overlap between schizophrenia, bipolar disorder and anxiety-related personality traits. In this study, we tested the hypothesis that the missence variation Thr136Ile in the VMAT1/SLC18A1 gene is associated with anxiety-related personality traits. We tested a total of 337 unrelated subjects of German descent (167 male, 170 female). All participants were carefully screened for psychiatric disorders. The self-report State–Trait Anxiety Inventory (STAI) was completed by all subjects. Genotypes were obtained for the Thr136Ile (rs1390938) variation in the VMAT1 gene for all subjects. Genotype effects on personality variables were computed with MANOVA including age as a co-variant and gender as independent factor (MANCOVA). Results show that STAI scores were significantly affected by genotype (F = 3.108; d.f. = 4,331; p = 0.015) and age (F = 7.233; d.f. = 2,331; p = 0.001) but not by gender. A gender-by-genotype effect was observed for both the STAI state (p = 0.052) and trait score (p = 0.035). Dissection of the group by gender and subsequent contrast analysis of the genotype effects performed within the female group showed significant results (STAI state: Thr/Ile vs. Ile/Ile: T = 4.408, p = 0.0004; STAI trait: Thr/Ile vs. Ile/Ile: T = 3.074, p = 0.009) but not in the male group. Our findings support the hypothesis that anxiety-related personality traits are associated with variation in the VMAT1/SLC18A1 gene.     

医科大学生焦虑情绪的心理社会因素探讨

目的探讨医科大学生焦虑情绪状态及其相关的心理社会因素。方法分层整群抽取某医科学校508名本科生进行焦虑情绪的流行特征及其相关因素的调查分析。结果医科大学生焦虑情绪检出率为9．03%，不同年级学生在SAS焦虑得分差异具有显著性，焦虑情绪与医科大学生的人格特征，特质应对方式、领悟社会支持、生活事件、父母文化程度、学生对专业满意程度和就业前景评价有高度相关性。结论应联合学校、家庭、社会，加强医科大学生心理健康教育；依据目标人群特点．采取有针对性的健康教育措施；着重塑造健康的性格，倡导应用积极的应对方式．提高适应环境能力，改善心理素质，以防止或降低其焦虑情绪的发生。     

综合性医院冠心病病人抑郁/焦虑现况研究

目的：了解综合性医院冠心病患者抑郁和／或焦虑症状患病率及既往诊治情况。方法：采用现况研究方法，于2004年6月1日到12月1日在北京、上海、广州和成都的7家综合性医院的心内科连续收集确诊的冠心病患者359例。由经培训的调查员用统一的调查表进行面对面调查，同时使用综合医院焦虑抑郁量表（HAD）、Hamilton焦虑量表和Hamilton抑郁量表进行心理测评。结果：冠心病患者的抑郁症状、焦虑症状、抑郁合并焦虑症状以及合计的抑郁和／或焦虑症状患病率分别为19．8％，16．7％，13．6％和22．8％；在具有抑郁和／或焦虑症状的非首诊患者中，冠心病患者既往被诊断为抑郁和／或焦虑障碍和接受抗抑郁和／或焦虑治疗的比例均低于4％：住院患者在本次住院期间的抑郁焦虑诊治率低于1％。结论：综合医院冠心病病人具有较高的抑郁和／或焦虑症状和抑郁和／或焦虑障碍患病率．且既往诊治率较低。     

焦虑性神经症患者投入超脱程度及相关因素研究

为了测量焦虑性神经症患者的认知 ,我们编制了精神超脱量表 ,并在大学生和社区人群中进行了信度和效度的检验[1] 。根据道家认知治疗的理论基础 ,焦虑性神经症患者应该存在认知偏差。那么这种偏差具体是什么 ,和患者的人格特征 ,A型行为特征和临床症状又有什么样的关系呢 ?为此我们对焦虑性神经症患者进行了对照研究 ,以验证在临床中发现的神经症患者的认知偏差及其临床意义。1　材料与方法1.1　研究对象患者来自 2 0 0 1年 2月至 2 0 0 2年 8月之间在某综合医院精神科门诊和某精神病院神经症病房就诊的焦虑性神经症患者 ,符合CCMD - 3中…     

Lack of functional estrogen receptor beta influences anxiety behavior and serotonin content in female mice

Estrogen has been linked to the modulation of anxiety in females. Here we report results of anxiety tests conducted in female estrogen receptor beta (ERbeta) knockout (ERbetaKO) and wild-type (WT) mice. Ovariectomized (OVX) mice treated with chronic estradiol (E2) replacement did not behave differently on the elevated plus-maze when compared with OVX mice that did not experience hormone replacement. However, a genotype difference was noted; WT females were more likely to explore the distal portion of the open arm of the maze than ERbetaKO littermates. In addition, ERbetaKO female mice had significantly lower serotonin (5-HT) content than WT littermates in several brain regions including: the bed nucleus of the stria terminalis, preoptic area, and hippocampus. A similar trend was noted in the dorsal raphe nucleus. Dopamine content was reduced within the caudate putamen in ERbetaKO mice as compared to brains from WT animals. Thus, in the absence of functional ERbeta, regardless of the presence or absence of circulating E2 in plasma, female mice exhibited enhanced anxiety and decreased concentrations of 5-HT or dopamine in several brain regions. We hypothesize that ERbeta is required during development to modulate the effects of estrogen on anxiety and catecholamine concentrations in female mouse brains.     

Pharmacological and clinical effects of buspirone

Clinical trials have demonstrated that buspirone (BuSpar) is effective in the treatment of anxiety with efficacy and dosage comparable to diazepam or chlorazepate. Buspirone has a unique structure and a pharmacologic profile which distinguishes it from the benzodiazepines. Because it lacks the anticonvulsant, sedative, and muscle-relaxant properties associated with other anxiolytics, buspirone has been termed "anxioselective." Animal studies suggest that it lacks potential for abuse, and this finding is supported by clinical investigations. Further preclinical work supports the contention that buspirone lacks liability to produce physical dependence or to significantly interact with central nervous system depressants such as ethanol. Moreover, biochemical investigations have not identified any direct interaction of buspirone with the benzodiazepine-gamma-aminobutyric acid-chloride ionophore complex. Pharmacologic studies on the molecular level indicate that buspirone interacts with dopamine and serotonin receptors. Recent behavioral, electrophysiological, and biochemical studies have clearly demonstrated that early hypotheses that buspirone might be considered a neuroleptic are no longer tenable. Recent evidence indicates that other neurotransmitter systems (serotonin, norepinephrine, acetylcholine) mediate buspirone's effects. It is hoped that future studies can define the mechanism by which buspirone alleviates the clinical manifestations of anxiety.