The Alterations in Expression of the Synaptophysin in Rat Brain Trauma Injury Model——an Experimental Study
Abstract
To study the rat brain trauma injury model and investigate the rules of transformation of expression of synaptophysin and its relationship between histology and radiology alternation after brain trauma injury. Methods 24 SD male rats aged three months were randomly divided into 4 groups, including a control group of 6 rats. The experimental group rats were received operation to build free falling brain trauma injury model. The rat were analyzed at 2, 4, 8 weeks after injury. The experimental group rat were killed after CT scan and functional evaluation, histological changes were measured through HE staining. Synaptophysin were observed by using immunofluorescence method and Western blot. Results After brain injury the functional evaluation of rat showed dysneuria. Edema and necrosis in neurons and local congestion at 24 h after injury, necrosis and solubility liquefaction at 2 weeks after injury, and histological defects at 4 weeks and 8 weeks after injury, were observed in HE staining in experimental group. The significant cerebral low density shadows at 24 h after injury, lightened in 2 weeks after injury, and disappeared at 4 weeks and 8 weeks after injury, left only the bone defects in CT images. Expression of synaptophysin in brain tissue was decreased from 2 weeks after injury and it was mild increased at 8 weeks after injury evaluated by immunofluorescence method and Western blot. Conclusion The functional evaluation, histological and CT scan result indicate that we have built the rat brain trauma injury model successfully. The damage of synapse was correlated with histological and radiological result. The expression of synaptophysin was decreased form acute stage and gradually increased until 8 weeks after injury. This study can be applied as control in research of nerve regeneration after brain trauma injury.
Keywords: Brain trauma injury, Animal model, Radiology, Histopathology
Full Text:
PDFReferences
FEENEY DM, BOYESON MG, LINN RT et al. Responses to cortical injury: I . Methodology and local effects of contusions in the rat. Brain Res,1981 ,211( 1) :67-77.
HOU ХЕ, DAHLSTROM A. Synaptic vesicle proteins and neuronal plasticity in adrenergic neurons. Neurochem Res, 2000,25(9/10)j1275-1300.
SONG SH, AUGUSTINE GJ. Synapsin Isoforms and Synaptic Vesicle Trafficking. Mol Cells, 2015, 38 ( 11 ); 936- 910.
CHEN J, YU S, FU Y, et al. Synaptic proteins and receptors defects in autism spectrum disorders. Front Cell Neurosci, 2014(8) :276[2015-11-09]. https://www. ncbi. nlm. nib. gov/ pmc/articles/PMC4161164/. doi: 10. 3389/fncel. 2014.
BEDERSONJB, PITTS LH. TSUJI M, et al. Rat middle cerebral artery occlusion: evaluation of the model and development of a neurologic examination. Stroke,1986 ,17(3): 472-476.
MARCHESAN JT, MORELLI T, MOSS K. et al. Association of Synergistetes and Cyclodipeptides with Periodontitis. J Dent Res,2015,94(10): 1425-1431.
CHAPPLE IL, GENCO R; working group 2 of the joint EFP/AAP workshop. Diabetes and periodontal diseases; consensus report of the Joint EFP/AAP Workshop on Periodontitis and Systemic Diseases. J Periodontol. 2013, 84 (4 Suppl): SI 06-SI 12.
ZHOU J, JIANG N, WANG S. et al. Exploration of human salivary microbiomes-insights into the novel characteristics of microbial community structure in caries and caries-free subjects. PLoS One, 2016, 11 ( 1 ): e0147039 [2015-11-03]. dx. doi. org/10. 1371/journal, pone. 0147039.
GURSOY UK, KONONEN E, PUSSINEN PJ, et al. Use of host- and bacteria-derived salivary markers in detection of periodontitis; a cumulative approach. Dis Markers, 2011, 30 (6):299-305.
ABUSLEME L, DUPUY AK, DUTZAN N, et al. The subgingival microbiome in health and periodontitis and its relationship with community biomass and inflammation. ISME J,2013,7(5); 1016-1025.
PARK OJ, YI H, JEON JH, et al. Pyrosequencing Analysis of Subgingival Microbiota in Distinct Periodontal Conditions. J Dent Res,2015,94(7):921-927.
GRIFFEN AL, BEALL CJ, CAMPBELL JH, et al. Distinct and complex bacterial profiles in human periodontitis and health revealed by 16S pyrosequencing. ISME J,2012,6(6); 1176-1185.
KISTLER JO. BOOTH V, BRADSHAW DJ, et al. Bacterial community development in experimental gingivitis. PLoS One»2013.8(8):e71227[2015-11-03]. http://dx. doi. org/10. 1371/journal, pone. 0071227.
HUANG S. YANG F, ZENG X. et al. Preliminary characterization of the oral microbiota of Chinese adults with and without gingivitis. BMC Oral Health. 2011 ( 11): 33 [2015-11-03]. http://www. ncbi. nlm. nih. gov/pubmed/ 22152152. doi: 10.1186/1472-6831-11-33.
ZORINA OA, PETRUKHINA NB, BASOVA AA, et al. Identification of key markers of normal and pathogenic microbiota determining health of periodontium by NGS- sequencing 16S-rI)NA libraries of periodontal swabs. Stomatologiia ( Mosk) ,2014 .93(6):25-31.
NAKANO K. MIYAMOTO E. NEMOTO H.et al. Clinical and microbiological evaluations of mandibular lateral incisor with radicular-gingival groove. Pediatric Dental Journal. 2007.17(1):93-99.
KIANOUSH N. ADLER CJ. NGUYEN KA, et al. Bacterial profile of dentine caries and the impact of pH on bacterial population diversity. PLoS One,2014 .9(3);e92940[2015-l 1- 03]. http://dx. doi. org/10. 1371/journal, pone. 0092940.
PAES BATISTA DA SILVA A, BARROS SP. MOSS K, et al. Microbial profiling in experimentally induced biofilm overgrowth among patients with various periodontal states. J Periodontol.2016.87( 1): 27-35.
Refbacks
- There are currently no refbacks.
