前额叶皮质星形胶质细胞与认知功能

背景 前额叶皮质是大脑的高级思维中枢,具有整合信息形成意识的重要功能,此功能主要由神经元之间的相互联系完成.星形胶质细胞占中枢神经系统的绝大多数,近期已有大量研究证明神经元与星形胶质细胞存在相互作用,但具体机制尚不明确. 目的 为某些神经性疾病的治疗和麻醉药物的应用提供重要思路. 内容 从病理学、生理学及行为学方面综述前额叶皮质星形胶质细胞与认知功能的关系.一些以认知功能损伤为主要表现的大脑损伤性疾病中,大脑前额叶皮质发生特征性改变的同时该区域星形胶质细胞功能异常,最终表现为明显的意识障碍. 趋向 星形胶质细胞主要通过钙振荡参与神经元的调控功能,但其具体机制仍需进一步研究探讨.     

脑缺血后星形胶质细胞能量代谢的改变:研究进展及临床意义

背景 星形胶质细胞是脑内重要的胶质细胞,对神经元的能量代谢、信号转导、电活动等方面都有重要的支持作用.脑缺血后星形胶质细胞能量代谢的变化,影响了神经元的存活和整个大脑的功能恢复. 目的 以星形胶质细胞能量代谢改变为切入点,探索治疗脑缺血疾病的新策略. 内容 从星形胶质细胞正常的能量代谢、缺血后星形胶质细胞能量代谢的改变、缺血引起能量代谢改变的可能机制以及临床意义4个方面进行综述. 趋向 为寻找基于星形胶质细胞的缺血早期干预和治疗措施提供新思路.     

Antagonists of the Vasopressin V1 Receptor and of the β1-Adrenoceptor Inhibit Cytotoxic Brain Edema in Stroke by Effects on Astrocytes – but the Mechanisms Differ

Brain edema is a serious complication in ischemic stroke because even relatively small changes in brain volume can compromise cerebral blood flow or result in compression of vital brain structures on account of the fixed volume of the rigid skull. Literature data indicate that administration of either antagonists of the V1 vasopressin (AVP) receptor or the β₁-adrenergic receptor are able to reduce edema or infarct size when administered after the onset of ischemia, a key advantage for possible clinical use. The present review discusses possible mechanisms, focusing on the role of NKCC1, an astrocytic cotransporter of Na⁺, K⁺, 2Cl^- and water and its activation by highly increased extracellular K⁺ concentrations in the development of cytotoxic cell swelling. However, it also mentions that due to a 3/2 ratio between Na⁺ release and K⁺ uptake by the Na⁺,K⁺-ATPase driving NKCC1 brain extracellular fluid can become hypertonic, which may facilitate water entry across the blood-brain barrier, essential for development of edema. It shows that brain edema does not develop until during reperfusion, which can be explained by lack of metabolic energy during ischemia. V1 antagonists are likely to protect against cytotoxic edema formation by inhibiting AVP enhancement of NKCC1-mediated uptake of ions and water, whereas β₁-adrenergic antagonists prevent edema formation because β₁-adrenergic stimulation alone is responsible for stimulation of the Na⁺,K⁺-ATPase driving NKCC1, first and foremost due to decrease in extracellular Ca²⁺ concentration. Inhibition of NKCC1 also has adverse effects, e.g. on memory and the treatment should probably be of shortest possible duration.     

星形胶质细胞在脑缺血损伤中的作用及其机制

背景 脑血管疾病严重危害人类健康,其中脑卒中是我国60岁以上人群致死第二大病因,同时因其高致残性愈发受到关注。先前脑保护研究主要针对神经元受损机制,而作为中枢神经系统中数量最多的星形胶质细胞,因其在构建中枢神经系统结构、辅助细胞间信号转导、调节神经元可塑性等过程中的重要作用,成为近年来脑保护治疗研究热点。目的 探究星形胶质细胞在脑缺血性损伤中的作用。内容 综述星形胶质细胞生理功能,星形胶质细胞在脑缺血性损伤中细胞形态和功能变化,星形胶质细胞神经保护作用。 趋向 星形胶质细胞有望成为脑缺血性损伤治疗的新靶点。     

渗透压变化对缝隙连接蛋白在培养的大鼠下丘脑星形胶质细胞和神经元表达的影响

目的观察渗透压改变对培养的下丘脑星形胶质细胞的缝隙连接蛋白Connexin43（Cx43）和神经元的缝隙连接蛋白Cx32表达的影响。方法体外培养孕14d或新生1d SD大鼠下丘脑的神经元和星形胶质细胞并进行纯化和鉴定。实验各分两组,第1组：细胞由等渗培养液移至高渗培养液（含9％NaCl）分别放置1min、3min、5min、10min和15min后将液体吸出常规固定;第2组：细胞先置于高渗培养液中15min后换成等渗培养液,分别在1min、3min、5min和10min后将等渗培养液吸出常规固定。两者均进行抗Cx43或抗Cx32的免疫荧光染色,Confoeal显微镜观察。结果第1组,Cx43在刺激1min后在星形胶质细胞表达比对照组有所增加,3min达到高峰,以后逐渐降低,15min恢复正常;而Cx32在刺激后1min的神经元中表达比对照组增加,5min达到高峰,以后降低。15min恢复正常。第2组同样为Cx43在星形胶质细胞刺激1min后表达增加,3min达到高峰,以后降低,10min恢复正常;神经元的Cx32表达在刺激后5min达到高峰,以后降低,10min恢复正常。两组Cx43表达的高峰期均早于Cx32。结论Cx43和Cx32可能参与星形胶质细胞与神经元渗透压的调节。