Evaluation of long term cognitive disorder after traumatic brain injury models by controlled cortical impact

Abstract

Objective To evaluate the method of controlled cortical impact(CCI) on long term cognitive disorder after traumatic brain injury(TBI)and to investigate the possible pathological mechanism. Methods Sixty male SD rats were randomly assigned into 3 groups : sham surgery group(n=10), control group (n=10) and CCI group(n=40). CCI application was used to make the bilateral frontal lobe controlled cortical impact model (depth: 1.5 mm, velocity=3.5 m/s, dwell time=400 ms). Morris water maze test and Nissl's staining was used to assess the cognitive function and pathological changes after 8 weeks of CCI. The expressions of brain derived neurotrophic factor (BDNF) and tyrosine protein kinase B (TrkB) mRNA in frontal lobe and hippocampus tissue was detected by reverse transcription polymerase chain reaction(RT-PCR). Results The mortality in CCI group was only 12.5%. Morris water maze test results showed the escape latency in CCI group was longer than that in sham surgery and control groups(F=51.784, P<0.05). Percent of time spend in goal quarter during probe trial in CCI group was significantly less than that in sham surgery and control groups(F=13.468, P<0.05). Nissl's staining showed frontal lobe had obviously defects; Nissl's bodies of frontal cortex and CA1 region in hippocampus reduced. The expressions of BDNF and TrkB mRNA in frontal lobe and hippocampus were significantly less than those in sham surgery and control groups(P<0.05). Conclusions The CCI model can be applied for study on long term cognitive disorder after TBI with good stability and repeatability. Using the experimental parameters of CCI can damage the long term cognitive function after TBI in rats, and lead the pathology changes of brain tissue clearly. This may have some relationship with the expressions of BDNF and TrkB mRNA. Key words: Animal model; Traumatic brain injury; Cognitive disorder; Brain derived neurotrophic factor; Tyrosine protein kinase B