Brain glycogen following experimental cerebral ischemia in gerbils (Meriones unguiculatus)

Summary Cortical glycogen levels decreased after both 1 and 3 h of unilateral ischemia. After 1 h of recirculation, the levels of glycogen were restored to control values in both groups. Subsequently, glycogen increased above normal levels after 1 week of recirculation in the 1 h ischemic groups, and after 5 h in the 3 h ischemic group. Thus, the onset of the excess glycogen accumulation appears to be dependent on the intensity of the ischemic insult.     

人类脑计划和神经信息学

人类脑计划是继人类基因组计划之后的又一重大科研计划,本文对该计划产生的历史背景,目的,现状,急需解决的问题作了简要的综述。     

脑功能成象的对话

介绍了现代脑功能成象技术,以及用脑功能成象技术研究脑的高级功能的方法。     

脑科学的前景展望

本文展望了脑科学若干领域的发展前景,包括神经活动的基本机制,脑的发育,神经和精神性疾病及脑的高级功能。     

Brain response to calorie restriction

Calorie restriction extends longevity and delays ageing in model organisms and mammals, opposing the onset and progression of an array of age-related diseases. These beneficial effects also extend to the maintenance of brain cognitive functions at later age and to the prevention, at least in rodents, of brain senescence and associated neurodegenerative disorders. In recent years, the molecular mechanisms underlying brain response to calorie restriction have begun to be elucidated, revealing the unanticipated role of a number of key nutrient sensors and nutrient-triggered signaling cascades in the translation of metabolic cues into cellular and molecular events that ultimately lead to increased cell resistance to stress, enhanced synaptic plasticity, and improved cognitive performance. Of note, the brain’s role in CR also includes the activation of nutrient-sensitive hypothalamic circuitries and the implementation of neuroendocrine responses that impact the entire organism. The present review addresses emerging molecular themes in brain response to dietary restriction, and the implications of this knowledge for the understanding and the prevention of brain disorders associated with ageing and metabolic disease.     

Brain microvessel hexokinase: Kinetic properties

Summary Kinetic differences between brain capillary and parenchymal hexokinase in the presence of glucose, ATP, fructose, potassium, sodium and different pH were established. Parenchymal hexokinase is more susceptible to glucose inhibition, can tolerate greater variations in the ATP concentration, is inhibited by increasing concentrations of fructose and potassium, and showed greater activity on the lower pH values. The data suggest that in brain parenchyma and endothelial cells of brain microvessels, there are 2 different enzymes with regard to the kinetic properties.     

Enzymuria following acute renal ischemia in dogs

Resumen Fue observado en los perros, nítido aumento en la excreción de transaminase glutamico-oxalo-acética, cininases y proteínas, inmediatamente después de una isquemia renal unilateral de 20 min. No fue observada ninguna alteración en la enzimuria o en la proteinuria en el riñon de control.

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Supported by U.S.P.H.S. Research grant No. HE-10074-02.     

Hepatic blood flow in acute myocardial ischemia

Hepatic blood flow was monitored in cats during myocardial ischemia (MI). Increased plasma CPK activity, the S-T segment of the electrocardiogram, and hepatic flow was reduced by 5 h to 40% of control. The results suggest that MI can influence organs distant from the original ischemic episode.     

Hepatic blood flow in acute myocardial ischemia

Summary Hepatic blood flow was monitored in cats during myocardial ischemia (MI). Increased plasma CPK activity, the S-T segment of the electrocardiogram, and hepatic flow was reduced by 5 h to 40% of control. The results suggest that MI can influence organs distant from the original ischemic episode.Supported in part by Research grant HL-17745 from the National Heart, Lung and Blood Institute of the National Institutes of Health.Acknowledgments. We gratefully acknowledge the expert technical assistance of Mary Ann Spath.     

异丙酚对大鼠内毒素脑损伤STAT3表达的影响

目的 研究异丙酚对大鼠内毒素脑损伤中信号转导子与转录激活子-3( STAT3)表达的影响,探讨异丙酚在脑损伤中的保护作用及其机制.方法 健康清洁级SD大鼠72只,雌雄不限,体重220～ 250 g,随机分为3组(n=24):L组(内毒素组)和LP组(内毒素+异丙酚组)经颈内动脉注射内毒素200 μg建立大鼠内毒素脑损伤模型,C组(对照组)经颈内动脉注射等量生理盐水,LP组颈内动脉注射内毒素后即予异丙酚100 mg/kg剂量腹腔注射.3组分别于6、12、24和48h随机处死6只大鼠,取额叶皮质,检测脑组织含水量,免疫组织化学检测P-STAT3、NF-κB和iNOS表达水平的变化,Western blot法检测大鼠内毒素脑损伤后P-STAT3蛋白表达水平的变化.结果 与C组相比,L组、LP组各时间点脑组织含水量、P-STAT3、NF-κB和iNOS表达增加(P ＜0.05,P＜0.01);与L组比较,LP组各时间点脑含水量、P-STAT3、NF-κB和iNOS表达明显减少(P＜0.05,P＜0.01).结论 异丙酚可减轻大鼠内毒素性脑损伤,机制可能与抑制脑组织磷酸化STAT3、NF-κB和iNOS表达水平上调,进而减轻炎性反应有关.     

Melatonin,mitochondria and hypertension

Melatonin, due to its multiple means and mechanisms of action, plays a fundamental role in the regulation of the organismal physiology by fine tunning several functions. The cardiovascular system is an important site of action as melatonin regulates blood pressure both by central and peripheral interventions, in addition to its relation with the renin–angiotensin system. Besides, the systemic management of several processes, melatonin acts on mitochondria regulation to maintain a healthy cardiovascular system. Hypertension affects target organs in different ways and cellular energy metabolism is frequently involved due to mitochondrial alterations that include a rise in reactive oxygen species production and an ATP synthesis decrease. The discussion that follows shows the role played by melatonin in the regulation of mitochondrial physiology in several levels of the cardiovascular system, including brain, heart, kidney, blood vessels and, particularly, regulating the renin–angiotensin system. This discussion shows the putative importance of using melatonin as a therapeutic tool involving its antioxidant potential and its action on mitochondrial physiology in the cardiovascular system.     

Brain microvessel hexokinase: kinetic properties.

Kinetic differences between brain capillary and parenchymal hexokinase in the presence of glucose, ATP. fructose, potassium, sodium and different pH were established. Parenchymal hexokinase is more susceptible to glucose inhibition, can tolerate greater variations in the ATP concentration, is inhibited by increasing concentrations of fructose and potassium, and showed greater activity on the lower pH values. The data suggest that in brain parenchyma and endothelial cells of brain microvessels, there are 2 different enzymes with regard to the kinetics properties.     

记忆过程的脑/心相关研究

本文首先介绍认知神经科学研究的实验范式,然后比编码／提取的非对称模型、启动效应的神经机制,情景记忆提取的两过程及其脑区和记忆是怎 的几个方面,介绍近年来认知神经科学关于记忆的研究。最后,强调了脑认和成象于心理学与脑科学的重要性。     

意识与脑内信息处理系统

本文从脑内的信息处理和系统科学观点讨论意识问题。首先提出脑内存在有意识和无意识活动以及意识问题的特点,在此基础上提出意识的脑机制的系统论观点,最后讨论了意识的困难问题以及意识与信息的关系。     

果蝇:基因、脑和行为

本文首先简单回顾了在果蝇研究历史中一些具有里程碑性的研究成果,然后着重介绍了以果蝇为实验模型所具有的诸多优势,以及在基因、脑、行为框架下的一些最新研究成果和未来的研究方向。     

Activation of cardiac vagal receptors during myocardial ischemia

Résumé La décharge de fibres vagales d'origine cardiaque est augmentée au cours d'une réduction du flux sanguin dans l'artère coronaire de gauche. Toutefois cette excitation n'a lieu que lorsque le coeur est déjà défaillant à cause de l'ichémie. La stimulation effective paraît être de nature mécanique.

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Aided in part by USPHS Grant No. Rol-HE-10977-05 and No. NS09545-01.     

Defective phosphoinositide metabolism in primary hypertension

An increase in free cytosolic calcium content has been reported in essential hypertension. Since within the membrane, the phosphoinositides participate in the control of cell calcium homeostasis, we investigated whether impaired phosphoinositide metabolism could account for the calcium handling abnormality observed in hypertensives. In erythrocyte membranes of hypertensives the activity of kinases involved in polyphosphoinositide formation appears to be impaired and could be related to the alteration in calcium handling binding capacity and ATP-dependent calcium transport. In platelets of hypertensives, the hyperactivity of phospholipase C (observed even in the absence of calcium in the external medium) is likely to be responsible for the hypersensitivity of cells to various agonists. These observations are consistent with the hypothesis that in cells from hypertensives, a membrane defect linked to phosphoinositide metabolism is involved in the overall calcium handling defect.