Study On Traumatic Brain Injury On Activation Of Calaium/calmodutin-dependent Protein Kinases In Rats Central Nervous System

Traumatic brain injury is a common complex disease，which threats to human health andlife seriously，ranks the first of brain disease mortality. More than five million people becomedisabled due to traumatic brain injury. Legacy of disability due to brain injury is an importanthealth concern topics. These disability or disease are due to primary injury or the laterdevelopment of secondary injury caused by focal or diffuse brain injury. Traumatic braininjury patients with typical pathological changes including contusion formation, nerve cellnecrosis and diffuse axonal injury. These pathological changes evolving in traumatic braininjury after a few hours to several days but also we need a potential target for therapy.Unfortunately, there is no effective drug treatment programs to treat those patients withtraumatic brain injury. According to Glasgow is classified into three grades, are light, medium,severe. The most common clinical traumatic brain injury is mild injury, Amnesia durationdoes not exceed24hours, Of course, there are more than50%of mild traumatic brain injurypatients with cognitive impairment is more than one year after head injury. The most commoncognitive impairment in learning and memory defects. Among them, In patients with mediumand severe traumatic brain injury are often accompanied by varying degrees of memoryimpairment. Although after traumatic brain injury brain tissue pathological changes have beenwell studied, to promote memory loss in the biochemistry of the mechanism is still not fullydepicted，especially in the following traumatic brain injury in hippocampal dependentmemory side has not been well explained. The present studies indicate that long termpotential (LTP) in memory formation plays an important role in. Because the CaMKs areone of the regulation of long term potential key protein, therefore this experiment study on thecentral nervous system calmodulin kinase as the research object, Study on the effects ofchanges in head injury.Objective:To explore effects of activation of calcium/calmodulin-dependent proteinkinases in Rats center nervous system after Traumatic Brain Injury. Provide a molecularmechanism that boost cells impaired plasticity after TBI, For the purpose of providing thepremise condition in clinical study of memory disorder occurrence mechanismin aftertraumatic brain injury. Methods:40adult male Wistar rats were distributed randomly to4groups: includesham,30min injury,6h injury and24h injury. The rats in injury group were made into braininjury model in the way of fluid percussion brain injury with pressure (200kPa),then killed therats at different time points The brains of rats were collected and fixed, embedded and sliced,observed changes of CaMKII activity in the parietal cortex and the hippocampus withImmunohistochemical and Western blot analysis. system analyze the activity of CaMKII withconfocal microscopy. All datas were observed by SPSS11.0analytical system, then analysisedstatistically with variance analysis and t test.Reasults:pCaMKII changes in neurons of the central nervous system after TBI.Plasma, axonal and synaptosome on the pCaMKII increased significantly at30min afterTBI (p <0.01); at6h after TBI began to decline, until the24h.Conclusions:Central nervous system phosphorylation of CaMKII expression quick increasedsignificantly and bind with synaptosome after TBI, then decreased in several hours.