创伤后应激障碍样行为异常大鼠海马钙/钙调素依赖性蛋白激酶IIá偄表达  

Expressions of Ca~ (2+)-CaM-CaMKIIá signaling in hippocampi of rats with PTSD-like behavior

作　　者：王庆松[1] 王正国[1] 朱佩芳[1] 

机构地区：[1]第三军医大学大坪医院野战外科研究所四室,重庆400042

出　　处：《中国行为医学科学》2002年第1期1-3,共3页Chinese Journal of Behavioral Medical Science

基　　金：国家自然科学基金资助项目 ( 39870 2 84);全军九.五医药卫生科研基金课题 ( 98M 0 44)

摘　　要：目的　探讨创伤后应激障碍 (PTSD)样精神与行为异常的神经生物学机制。方法　在大鼠海马惊厥阈下电刺激PTSD动物模型基础上 ,采用流式细胞仪、荧光标记术及Westernblotting等方法 ,定量观测了PTSD样行为异常大鼠海马细胞内游离Ca2 + 含量与钙调素 (CaM )相对活性平均通道荧光 ,及海马组织总CaM、Ca2 + /CaM依赖性蛋白激酶II偄(CaMKII偄)表达的动态变化规律。结果　电刺激停止后 72h内阈下刺激组实验动物海马细胞内游离钙浓度明显增高 ,游离CaM平均通道荧光则同步降低 ;而海马组织总CaM表达于电刺激停止后 48h内明显增多 ,CaMKII偄表达则显著降低?崧邸『B硐赴鸆a2 + CaM CaMKII偄信号途径调控紊乱可能是实验动物长时程ＰＴＳＤ样行为异?Objective To explore the neurobiological bases in the pathogenesis of the lasting emotional behavioral disorders following posttraumatic stress disorder (PTSD).Methods After establishing the PTSD animal model of subconvulsive stimulation to hippocampus, the intracellular free calcium by Fura-2/AM, free calmodulin (CaM) by flowcytometry, and the total CaM and Ca 2+/CaM dependent kinase II á (CaMKIIá) by Western blotting were detected in hippocampi of experimental rats.Results The intracellular free calcium levels were increased, and the Mean Channel Fluorescence of intracellular free CaM decreased remarkably in 72 h poststimulation, while the expression of total CaM was significantly elevated in 48 h after the last stimulation, and that of CaMKIIá was markedly decreased as well in hippocampi of experimental rats with PTSD-like behavior.Conclusion It indicated that the dysfunction of Ca 2+-CaM-CaMKIIá signaling pathway in hippocampi may play an important role in the long-term neuropsychological sequelae in rats with PTSD-like behavior.

关 键 词：应激障碍 创伤后 海马 钙 钙调素 CAMKIIΑ 

分 类 号：R363[医药卫生—病理学]