目的观察慢性脑缺血大鼠海马组织蛋白激酶C(protein kinase C,PKC)、钙调素依赖蛋白激酶Ⅱ(calmodulin-depend-ent protein kinaseⅡ,CaMKⅡ)水平变化,探讨其在慢性脑缺血认知功能损害中的作用。方法采用双侧颈总动脉永久性结扎(per-manent occlusion of bilateral common carotid arteries,2-VO)制作慢性脑缺血模型,40只大鼠随机分为假手术组,缺血3周组,缺血8周组,缺血12周组(n=10),Morris水迷宫检测大鼠空间学习记忆能力,Western blot法检测大鼠海马神经元PKC、CaMKⅡ、谷氨酸受体NMDAR1、NMDAR2B的表达水平,并观察其动态变化过程。结果缺血3周组大鼠的空间学习记忆能力较假手术组显著下降(P<0.05),缺血8周和12周组下降更加明显(P<0.01)。缺血3周组海马区PKC、CaMKⅡ与谷氨酸受体NMDAR 1、NMDAR 2B表达水平较假手术组增高(P<0.01),缺血8周和12周组表达均降低(P<0.01)。结论PKC、CaMKⅡ与谷氨酸受体NMDAR 1、NMDAR2B变化规律相同,在缺血后期PKC、CaMKⅡ表达减低可能与学习记忆损害有关。
Gap junction is one kind of synapse coexisting with chemical synapse in the nervous system. Nowadays with the development of electrophysiological technique,more research began to focus on the role of gap junction in the neural network,especially in the cognitive function. Gap junction collaborates with chemical synapses to induce the neural network activities related to memory and perception,such as gamma and ripple oscillation,which is regarded as the mechanism of the role of gap junction in cognitive function. This review introduces the structure of gap junction,distribution and expression of different kinds of connexins in central nervous system,which are the basic element of gap junction. Furthermore,this review discusses the role of gap junction in cognition related network oscillations and activity-dependent plasticity of gap junction.
