A Study On Molecular Mechanism Of Cognitive Deficits After Traumatic Brain Injury

Objective To establish model of traumatic brain injury rats, investigate the morphological and quantitative changes of pyramidal neurons in hippocampal of TBI rats, observe the feature of cognitive dysfunction and the changs of postsynaptic density 95(PSD-95) and the actin-related protein-2/3(ARP2/3) complex, to study the relationship between cognitive deficits and synaptic plasicity in traumatic brain injury rats, analyse molecular mechanism of cognitive deficits after traumatic brain injury and provide objective molecular biological bases for clinical diagnosis and treatment related to traumatic brain injury.Methods A total of 80 adult male Sprague-Dawley rats were randomly assigned to sham group(n=35) and injured group(n=45). A traumatic brain injury was produced in rats using the impact acceleration model. Random select sham group(n=10)and injuryed group(n=10)that using Morris Water Maze(MWM) memory paradigm to assess learning and memory function. The diameter and number of branch of apical dendrites of the sham(n=12) and injury(n=12) hippocampal pyramidal neurons were measured by using Golgi staining. Protein electrophoresis(Western Bolt) was used to observe the expression of postsynaptic density 95(PSD-95) and the actin-related protein-2/3(ARP2/3) complex after injured 1day(n=5),3day(n=5),7day(n=5).Results Compared with the control group, the latency to find the platform of the Morris Water Maze test in the 1st~7th day post traumatic brain injury much longer than that in the control; The number of dendritic shaft of the hippocampal pyramidal neurons was significantly decrease, the diameter of branch was not change;The expression of postsynaptic density-95(PSD-95) and the actin-related protein-2/3(ARP2/3) complex both reduce. Moreover, the decrease of density-95(PSD-95) and the actin-related protein-2/3(ARP2/3) complex related to the time of the trumatic brain injury.Conclusions 1.The spstial learning and memory deficits of the rats are detected by MWM in early period post traumatic brain injury(from 1 to 7 days after traumatic brain injury); 2. The number of dendritic shaft of the hippocampal pyramidal neurons was decrease; 3. The expression of postsynaptic density-95(PSD-95) decrease in traumatic brain injury; 4. The expression of actin-related protein-2/3(ARP2/3) complex decrease in traumatic brain injury; 5. Synaptic plasicity correlate with cognitive deficits in traumatic brain injury rats.