人格生物学基础研究的某些进展

本文综述了20世纪90年代以来关于人格的遗传力估计、多巴胺基因和5-羟色胺基因对人格特质的影响和人格的神经科学基础等方面的研究进展。认为人格特质的表现受多种基因控制,是通过生物学系统的活动实现的,并且是生物学过程和环境影响交互作用的结果。     

多巴胺与运动能力的关系

多巴胺主要生理功能是调节躯体运动、神经活动等。脑中的多巴胺合成和分解与运动能力有密切的关系,其含量的增加可以提高运动能力,尤其是耐力运动能力,多巴胺还可以通过调节其他激素以及影响心血管来影响运动能力;多巴胺也与运动性中枢疲劳有联系;多巴胺合成和分泌异常与帕金森综合征并伴有迟发型运动障碍有关。本文对多巴胺与运动能力之间的关系做一综述。     

中等强度有氧运动大鼠环境应激的保护效应及其机制探讨

通过观察经中等强度有氧运动后大鼠对损害性应激的反应变化及神经内分泌改变,探讨中等强度有氧运动对大鼠应对外界损害性应激能力的影响及其机制。     

多巴胺在聚L-谷氨酸修饰碳黑微电极上的电催化氧化

研究了聚L-谷氨酸修饰碳黑微电极的制备及多巴胺在该电极上的电化学性质。实验表明:该修饰电极对神经递质多巴胺的电化学氧化有显著的催化作用,采用二次导数线扫伏安法对多巴胺进行定量分析,线性范围为1.0×10-4~4.0×10-8mol/L,检出限为8.0×10-9mol/L。该聚合物修饰电极具有良好的选择性,能有效地排除抗坏血酸对测定的影响,用于样品分析,结果满意。     

多巴胺与去甲肾上腺素在感染性休克中的应用研究

感染性休克是一种复杂的高病死率的临床综合征,是重症监护病房最常见的死亡原因之一,严重威胁着人类的健康。多巴胺和去甲肾上腺素对肾脏及其他器官均产生重要的影响,可以作为一线升压药物。传统的观点认为去甲肾上腺素具有减少肾脏及胃肠道黏膜的血液灌注等不良作用,然而,近来却发现,去甲肾上腺素应用于感染性休克,对于肾脏、胃肠道、心血管系统、呼吸系统及机体免疫系统都具有重要的作用。     

Sympathoadrenal and parasympathetic responses to exercise

Exhaustive exercise is associated with a persistent sensation of weakness and sometimes nausea suggesting abdominal vagal activity. We measured plasma indices of sympathoadrenal (adrenaline, noradrenaline, dopamine) and vagal (pancreatic polypeptide) activity before, during and after submaximal and maximal exercise in healthy young subjects. Plasma adrenaline, noradrenaline and dopamine increased to 8.5 (range 7.4–40.5), 48.0 (32.3–100.5) and 1.8 (1.2–6.6) nmol l^–1 respectively (n = 5), during maximal exercise and decreased towards control values within 15 min of rest. Pancreatic polypeptide (n = 10) increased only during maximal exercise and reached its highest value, 48 (21–145) pmol l^–1, after exertion. The results conform to an increase in sympathetic activity during exercise and a persistent vagal activity after intense exercise which could contribute to the sensation of weakness.     

Central dopaminergic neurotransmission plays an important role in thermoregulation and performance during endurance exercise

Dopamine (DA) has been widely investigated for its potential role in determining exercise performance. It was originally thought that DA's ergogenic effect was by mediating psychological responses. Recently, some studies have also suggested that DA may regulate physiological responses, such as thermoregulation. Hyperthermia has been demonstrated as an important limiting factor during endurance exercise. DA is prominent in the thermoregulatory centre, and changes in DA concentration have been shown to affect core temperature regulation during exercise. Some studies have proposed that DA or DA/noradrenaline (NA) reuptake inhibitors can improve exercise performance, despite hyperthermia during exercise in the heat. DA/NA reuptake inhibitors also increase catecholamine release in the thermoregulatory centre. Intracerebroventricularly injected DA has been shown to improve exercise performance through inhibiting hyperthermia-induced fatigue, even at normal ambient temperatures. Further, caffeine has been reported to increase DA release in the thermoregulatory centre and improves endurance exercise performance despite increased core body temperature. Taken together, DA has been shown to have ergogenic effects and increase heat storage and hyperthermia tolerance. The mechanisms underlying these effects seem to involve limiting/overriding the inhibitory signals from the central nervous system that result in cessation of exercise due to hyperthermia.     

碳纳米管修饰电极对多巴胺的电催化

制备了羧基化多壁破纳米管修饰电极．考察了该电极在PH=5．4的0．2mol／L的KH2PO4-Na2HPO4磷酸盐缓冲溶液中的电化学行为．结果显示该电极对其电极上的反应具有明显的促进作用并对生物分子多巴胺具有明豆电催化作用．     

基底神经节与口吃

本文回顾了口吃和基底神经节功能障碍之间关系的相关文献,从基底神经节的时间线索功能缺陷、基底神经节运动环路的损伤、多巴胺系统异常等三个方面系统探讨了口吃者基底神经节功能障碍的机制。     

Kir6.2构成的ATP敏感性钾通道在苯环己哌啶诱导的精神分裂症阴性症状中的作用

目的:ATP敏感性钾(K-ATP)通道对多巴胺和谷氨酸能传导具有重要的调节作用,而多巴胺和谷氨酸能传导之间相互作用是精神分裂症病理机制的重要神经化学基础.因此,我们应用Kir6.2(主要表达在神经元的K-ATP亚基)敲除小鼠,通过苯环己哌啶诱导强迫游泳不动时间的延长,模拟精神分裂症的阴性症状,从而研究K-ATP通道在其中的作用.方法:连续注射14d苯环己哌啶(10 mg·kg-1,i.p.)后,通过观察强迫游泳实验中小鼠不动时间的长短,评价Kir6.2敲除对精神分裂症阴性症状中抑郁样表现的影响;应用高效液相色谱联合电化学检测法观察纹状体多巴胺及其代谢产物、多巴胺更新率的改变;应用溴脱氧尿嘧啶核苷插入法观察海马齿状回颗粒下区神经干细胞增殖的改变;应用Western blot技术观察磷酸化Akt水平的变化.结果:Kir6.2敲除取消了苯环己哌啶引起的强迫游泳不动时间的延长.不仅如此,Kir6.2敲除还抑制了苯环己哌啶诱导的纹状体多巴胺更新率的增加、海马齿状回颗粒下区神经干细胞增殖的减弱,以及磷酸化Akt水平升高.结论:Kir6.2组成的K-ATP通道参与了苯环己哌啶诱导的精神分裂症阴性症状,阻断K-ATP通道有望成为治疗精神分裂症的新策略.