发育中脑惊厥性损伤与海马Zn^(2+)转移  

Seizure-induced Brain Injury in Brain Development and Zn^(2+) Metastasis in Hippocampus

作　　者：倪宏[1] 

机构地区：[1]苏州大学附属儿童医院儿科研究所,苏州215003

出　　处：《生理科学进展》2006年第4期331-334,共4页Progress in Physiological Sciences

基　　金：国家自然科学基金(30470555);中国博士后科学基金(2003034094)资助课题

摘　　要：Zn2+是一种新的调节神经系统兴奋毒性损伤的离子型介质。积聚于海马苔藓纤维(MF)通路突触前膜囊泡内的Zn2+,通过特定的自稳态机制向突触后神经元转运,以此实现对大脑兴奋-抑制平衡和认知功能的调节作用。发育中长程或反复惊厥造成海马MF通路Zn2+的自稳态破坏,Zn2+在细胞内和突触间发生异常转移,并有再生性发芽等病理损伤现象。Zn2+转运体、Ca2+通透性α-氨基-3-羧基-5-甲基异恶唑-4-丙酸(AMPA)/红藻氨酸通道(Ca-A/K通道)、金属结合蛋白和线粒体等共同参与发芽过程中Zn2+的异常转移。除此之外,Zn2+亦可作为神经调质,激活信号转导通路,对突触的功能或可塑性产生微妙的影响。这一独特的离子型跨突触信使作用可能具有重要的生理和病理意义。Zn^2＋ is a novel ionic mediator of neurotoxic injury in central nervous system. Zn^2＋ homeostasis in hippocampal Zinc-rich mossy fiber （MF） pathway is important in keeping the balance between excitatory and inhibitory system, and in maintaining cognitive functions of the brain. Abnormal Zn^2＋ metas- tasis occurred during MS sprouting induced by developmental seizures and influenced the function of hippocampus. The Zn^2＋ transporters, Ca^2＋ permeable AMPA/kainate channels, metal binding proteins and mitochondrion may involved in this process. In addition to pathological effects of rapid intraneuronal Zn^2＋ accumulation, it is probable that following lower exposures, activation of signaling pathways by intracellular Zn^2＋ has important yet largely obscure effects on physiological synaptic functioning or synaptic plastic- ity. This unique ionic trans-synaptic messenger probably plays important roles in normal physiological functioning as well as in disease. Further elucidation of the process of Zn^2＋ metastasis in hippocampus should yield breakthroughs both in understanding the mechanism of developing seizure-induced brain injury and contributing the effects for making proper early intervention.

关 键 词：海马 发育 惊厥 ZN^2+ 

分 类 号：R338[医药卫生—人体生理学]