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Objective:To investigate the effects of esketamine on the behavior of post-traumatic stress disorder(PTSD).Methods:Thirty-six adult male SD rats were randomly divided into three groups. The mouse craniocerebral trauma model was established by cortical impact injury method. The Sham group ( n=12) only opened the bone window without craniocerebral trauma. The TBI group( n=12) and the TBI+ ES group( n=12) were subjected to cortical trauma; Immediately after trauma, the TBI+ ES group was intraperitoneally injected with esmketamine (10 mg/kg, once every two hours, three times in total), and the TBI group and Sham group were intraperitoneally injected with equal volume 0.9% sodium chloride solution. The results of sugar water preference test, open field test on day 16 and elevated cross maze test on day 17 were collected to analyze PTSD like behavior changes, and Morris water maze test was used to evaluate the learning and memory ability of rats in each group from day 18 to 23 after craniocerebral trauma. After the experiment, the rats were euthanized and the brain tissues were taken. The expression levels of brain-derived neurotrophic factor (BDNF), synaptic protein PSD95 and synaptophysin (Syp) were analyzed by Western blot. The measurement data of normal distribution were expressed as mean ± standard deviation ( ± s). One way ANOVA was used for multi group comparison, SNK- q test was used for post pairwise comparison, and LSD method was used for repeated measurement data. Results:In the TBI group, the preference rate of sugar water, the number of moving grids, the number of standing upright, the residence time of open arm, the number of open arm entry, the escape latency and the number of crossing platform [(75.8±4.9)%, (30.9±4.1) grids, (12.4±2.6) times, (40.3±8.5) s, (6.8±2.3) times, (30.0±4.6) s and (7.0±2.5) times] were significantly lower than Sham group [(85.3±4.4)%, (40.5±5.4) grid, (17.3±2.7) times, (95.8±12.4) s, (15.3±3.1) times, (18.3±7.8) s, (15.7±2.6) times] ( P< 0.05); In TBI+ ES group, the sugar water preference rate, the number of moving grids, the number of upright times, the time of open arm stay, the number of open arm entry, the number of escape latency and the number of crossing platform position [(82.9±5.5)%, (35.5±5.5) grids, (15.1±2.4) times, (68.4±9.7) s, (12.1±3.2) times, (22.3±8.8) s and (12.5±4.1) times] were significantly higher than those in TBI group ( P<0.05). The expression levels of BDNF, PSD95 and Syp in TBI+ ES Group [0.43±0.08), (0.22±0.02), (0.31±0.04)] were higher than those in TBI group [0.19±0.02), (0.20±0.02), (0.24±0.01)], the difference was significant ( P<0.05), and they were lower than those in Sham group [0.89±0.11), (0.45±0.12), (0.57±0.15)], and the difference was significant ( P<0.05). Conclusion:Esticketamine significantly reduce PTSD-like behavior in TBI rats and play a neuroprotective role, which may be a potential medicinefor PTSD treatment.
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Objective To explore the correlation between the changes of mitochondrial DNA (mtDNA) copy number of peripheral blood leukocytes and the degree of neurological impairment after traumatic brain injury (TBI).Methods A total of 40 Sprague Dawley rats were randomly divided into 4 groups:control group (n=10),mild TBI group (n=10),moderate TBI group (n=10) and severe TBI group (n=10).The cortical impact injury method to construct TBI rat model of different damage degree.The neurological score (mNSS,screen test,open field test) after TBI 24 h,48 h,72 h was performed and the orbital venous plexus blood genomic DNA was extracted.The real-time PCR method to measure the relative mitochondrial DNA copy number.After the experiment,the rats were euthanized,and the brain tissue was stained with hematoxylin-eosin staining(HE).Results There were significant differences in the HE staining findings of brain tissue pathology (P＜ 0.05).Each group of rats with brain injury after peripheral blood mtDNA copy number in 24 h (9.63±3.62,P＜0.05) and 48 h (9.80±3.58,P＜0.05) increased,began to decline at 72 h (4.97±2.68,P＜0.05).The rats mNSS scores were related with the mtDNA copy number after TBI 24 h (r=0.578,P＜0.05) and 48 h (r=0.559,P＜0.05),and not related to TBI 72 h (r=0.487,P＞0.05).The rats screen test scores were related with the mtDNA copy number after TBI 24 h (r=0.573,P＜0.05) and 48 h (r =0.501,P＜0.05),and not related to TBI 72 h (r=0.273,P＞0.05).The rats level scores of open field test were negatively correlated with the mtDNA copy number after TBI24 h (r=-0.662,P＜0.05) and 48 h (r=-0.507,P＜0.05),and not negatively correlated to TBI 72 h (r=-0.410,P＞0.05).The rats vertical scores of open field test were negatively correlated with the mtDNA copy number after TBI 24 h (r=-0.662,P＜0.05)and 48 h (r =-0.607,P＜ 0.05),and not negatively correlated to TBI 72 h (r =-0.141,P＞ 0.05).Conclusion TBI is related with the copy of early peripheral white blood cell number and mtDNA of rat nerve function damage,and mtDNA copy number of peripheral white blood cell may become a clinical evaluation of TBI neural function damage degree of a potential biomarker.
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The study of brain-machine interfaces ( BMI) based on humans or animals is expected to improve the living conditions of patients with brain injury, nervous system disease and limb movement disorders.Considerable progress has been made over the past ten years, which is gradually being used to address the long-term and stability issues of BMIs technology.The result of study on safety and security of BMIs has led to the appearance of brain control animals.In this paper, the development of BMI technology and the application prospects of brain control animals are reviewed.