一重和三重脑震荡鼠八臂迷宫参考记忆与工作记忆动态变化和中枢变性细胞定量研究

【作者】 曹珍珍；

【导师】 于建云； 郭泽云； 瞿勇强；

【作者基本信息】 昆明医学院 ， 法医学， 2010， 硕士

【摘要】 【摘要】目的：探讨一重和三重脑震荡后24天内学习记忆能力的动态改变。方法：成年SD大鼠30只,应用单摆式闭合性脑损伤机械打击装置,复制不同损伤程度的脑震荡大鼠,随机分为PCC和MCC伤后组(n=8),应用八臂迷宫试验观测评价大鼠伤后学习记忆能力。结果：与正常组比,(1)伤后摄取食物量下降,PCC组1-11d(0.00±0.00至2.62±1.76)、MCC组1-24d(0.00±0.00至0.75±1.48)均有统计学意义(t≥3.75,P<0.05)：(2)伤后精神运动抑制即入臂总次数下降,PCC组1-7d、13d(4.87±1.24至10.0±2.39)、MCC组1-8d、22d(4.25±5.03至9.37±4.20)有统计学意义(t≥3.75,P<0.05)：(3)伤后参考记忆即入有食物臂次数先降后恢复,PCC组1-7d(0.50±0.75至3.00±1.06等)、MCC组1-19d(1.88±2.10至2.50±2.44)有统计学意义(t≥3.50,P<0.05)：(4)工作记忆即重复入无食物臂的次数出现延迟性损伤,PCC组1-6d、10-23d(0.00±0.00至4.25±3.05)、MCC组1-4d、6d、9-13d、15-16d、19-22d(0.25±0.46至3.12±2.87)有统计学意义(t≥3.52,P<0.05)。结论：一重和三重脑震荡鼠在八臂迷宫实验中,摄食功能、精神运动、参考记忆与工作记忆在伤后不同时间表现出严重受损,且前三者的损伤程度与脑震荡损伤次数呈正相关。摘要】目的：建立PCC和MCC大鼠模型，通过固缩的神经元、大胶质细胞(macroglia)、小胶质细胞(microglia)数目的变化规律，观察PCC、MCC大鼠大脑病理形态学的变化规律。进一步探讨CC大鼠认知行为障碍的神经生物学基础，并探讨PCC和MCC是否有损伤积累效应。方法：用自制金属单摆式闭合性脑损伤打击装置复制PCC和MCC大鼠模型96只，随机分为PCC大鼠伤后1d、2d、4d、8d、16d、24d和MCC大鼠1d、2d、4d、8d、16d、24d(n=6)十二个实验组，另设一正常对照组(n=6)。运用HE、尼氏染色方法分别进行组化染色，对中隔断面染色图片的前额叶皮质(PFC)、第一躯体感觉皮质(S1FL)、梨状皮质(Pir)、嗅结节(Tu)、尾壳核(CPu)、外侧隔核(LSD)、终纹床核(BST)、外侧隔核腹侧区(LSV)，背侧海马断面染色图片的压部无颗粒细胞皮质(RSA)、第一躯体感觉皮质(S1Tr)、梨状皮质(Pir)、海马CAl-4区(CAl-4)、上齿状回、下齿状回、丘脑背外侧核(LD)、皮质后外侧杏仁核(PLCo)；脑干断面图片的脑桥平面、斜方体平面、橄榄核平面以及被盖区等23个脑区进行固缩神经元、大胶质细胞、小神经胶质细胞分别计数。结果：(1)CC后各脑区固缩的神经元数目均呈现上升趋势：与正常组相比，PCC组中隔PFC、S1FL、中隔Pir、RSA的高峰在8d和24d，Tu的高峰在16d，CPu、LSV、脑桥平面、斜方体平面、橄榄核平面以及被盖区的高峰在8d，LSD的高峰在1d和4d，BST、LD的高峰在1d和8d、S1Tr的高峰在1d和24d、海马Pir的高峰在16d、CA1、CA2、CA3、CA4、上齿状回、下齿状回的高峰在8d，PLCo的高峰在1d和4d；MCC组中隔PFC、S1FL、中隔Pir、RSA的高峰在8d和24d，Tu、海马Pir的高峰在16d，CPu、LSV、CA1、CA2、CA3、CA4、上齿状回、下齿状回、脑桥平面、斜方体平面、橄榄核平面以及被盖区的高峰在8d，LSD、BST、LD的高峰在1d和8d，S1Tr的高峰在1d和24d，PLCo的高峰在1d和4d。(2)CC大鼠伤后各脑区大胶质细胞数均呈先略下降后上升趋势：PCC组与正常组相比中隔PFC的低谷在1d高峰24d，S1FL、中隔Pir、Tu的低谷在1d高峰16d，CPu低谷在1d高峰在8d，LSV、BST、海马Pir、LD、脑桥平面、斜方体平面、橄榄核平面以及被盖区的低谷在2d高峰在16d，LSD的低谷在4d高峰在8d，RSA、S1Tr的低谷在2d和16d高峰在8d，CA1、CA2、CA3、CA4的低谷在2d和24d高峰在8d，上齿状回、下齿状回的低谷在1d和24d高峰在8d，PLCo的的低谷在2d高峰在8d；MCC组中隔PFC的低谷在2d高峰24d，S1FL、CPu低谷在1d高峰8d，中隔Pit低谷在4d高峰16d、Tu的低谷在1d高峰16d，LSV、BST、海马Pit、脑桥平面、斜方体平面、橄榄核平面以及被盖区的低谷在2d高峰在16d，LSD、RSA、S1Tr、PLCo的低谷在2d高峰在8d，CA1、CA2、CA3、CA4的低谷在2d和24d高峰在8d，上齿状回、下齿状回的低谷在1d和24d高峰在8d，LD的低谷在1d高峰在16d的。(3)CC大鼠伤后各脑区小胶质细胞数均呈上升趋势：与正常组相比，PCC组中隔PFC的高峰在8d和24d，CPu、LSV、LSD、S1FL、RSA、海马Pir、CA1、CA2、CA3、CA4、上齿状回、下齿状回、PLCo、脑桥平面、斜方体平面、橄榄核平面以及被盖区的高峰在8d，中隔Pir、Tu、BST、S1Tr的高峰在16d，LD的高峰在1d和16d；MCC组中隔PFC、S1FL、中隔Pir、RSA的高峰在8d和24d，Tu、海马Pir的高峰在16d，CPu、LSV、CA1、CA2、CA3、CA4、上齿状回、下齿状回、LD、脑桥平面、斜方体平面、橄榄核平面以及被盖区的高峰在8d，LSD、BST的高峰在1d和8d，S1Tr的高峰在1d和24d，PLCo的高峰在1d和4d。结论：(1)CC后各脑区固缩的神经元数目均呈现上升趋势。(2)CC大鼠伤后各脑区大胶质细胞数均呈先略下降后上升趋势。(3)CC大鼠伤后各脑区小胶质细胞数均呈上升趋势。更多还原

【Abstract】 [Abstract] Objective:To observe learning and memory behavior changes of one time cerebral concussion called pure cerebral concussion (PCC) and three times cerebral concussion called multiple cerebral concussion (MCC) after injured 24 days in rats. Methods:A metallic pendulum striker device was deployed to duplicate PCC and MCC model in SD rats which are the complete closed head injury model. The animals were divided into PCC and MCC groups at random. One control group was used, each group has eight animals (n=8). One 8-arms radial maze was used to assessed each animal’s capabilities, that is, spatial reference memory, working memory, spirited activity and take in food. Result:Compared with control group, there are some significance(P＜0.05) in both experiment groups post injury, that is, (1) The food intake decreased, PCC group from the 1st to the 11th day (from 0.00±0.00 to 2.62±1.76) after injury, MCC group from the 1st day to the 24th day(from 0.00±0.00 to 0.75±1.48) after injury.(2)Spirited activity depressed, PCC group on the 1st to the 7th,13rd day(from 4.87±1.24 to 10.0±2.39) after injury, MCC group on the 1st to 8th、22nd day(from 4.25±5.03 to 9.37±4.20) after injury. (3)The spatial reference memory was lower in early then gradually increased, PCC group on the 1st to 7th day (from 0.50±0.75 to 3.00±1.06) after injury, MCC group from the 1st to 19th day(from 1.88±2.10 to 2.50±2.44) after injury.(4)The working memory was delaying damaged, PCC group from the 1st to the 6th day and the 10th to the 23rd day(from 0.00±0.00 to 4.25±3.05) after injury, MCC group on the 1-4th,6th,9-13th,15th,16th,19th-22nd day (from 0.25±0.46 to 3.12±2.87) after injury. Conclusion:The injured rats’capability of spatial reference memory, working memory, spirited activity and food intake were obviously damaged after CC, and the MCC group’s capability of spatial reference memory, spirited activity and food intake was worse than PCC group. [Abstract] Objective: To establish the model of pure cerebral concussion(PCC) and multiple cerebral concussion(MCC) in rats, observe the number of pyknosis neurons, macroglias and microglias post-PCC and post-MCC. so as to understand the neurobiologic mechanisms of cognitive behavioral dysfunction after PCC and MCC in rats. To explore if MCC can increase the injury compared with PCC. Methods: The PCC or MCC model was duplicated by using a metallic pendulum-striker concussive devicye. 96 female and male Sprague—Dawley rats were randomly divided into tweleve groups: PCC1d,2d,4d,8d,16d,24d group and MCC1d,2d,4d,8d, 16d,24d group (n=8,in each group). One control was used (n=8). Using the Hematoxylin and Eosin staining (HE) method and Nissl staining method to detect the numbers of neurons, macroglias and microglias in the following areas, that is PFC, S1FL, Pir, Tu, Cpu, LSD, BST, LSV, PFC, S1Tr, Pir, CA1, CA2, CA3, CA4, dentate gyrus, under the dentate gyrus, LD, PLCo, pons, trapezoid body, olive and PR. Result: (1) The number of pyknosis neurons in cerebral cortex was increased post-injury and declined then. Comparered with control, septal PFC, S1FL, septal Pir, the hippocampus PFC peak of PCC in 8d 24d, Tu peak in 16d, CPu, LSV, the pons plane, oblique side plane, olive tegmental area flat and the peak in the 8d , LSD peak at 1d and CA1, CA2, CA3, CA4, the dentate gyrus, dentate under back to the peak in the 8d, PLCo peak at 1d and 4d;and Septal PFC, S1FL, septal Pir, the hippocampus PFC peak of MCC in 8d and 24d, Tu, Pir hippocampus of the peak in 16d, CPu, LSV, CA1, CA2, CA3, CA4, the dentate gyrus, under the dentate gyrus, pons plane, oblique plane, olive tegmental area flat and the peak in the 8d, LSD, BST, LD peak at 1d and 8d, S1Tr peak at 1d and 24d, PLCo peak at 1d and 4d. (2)The number of macroglias was declined post-injury and increased then. Comparered with control, the low of septal PFC in PCC was in the 1d and peak 24d, S1FL, septal Pir, Tu’s low was 1d and peak 16d, CPu low was 1d peak 8d, and the low of LSV, BST, hippocampus Pir, LD, flat pons, trapezoid body plane, olive tegmental area of nuclear surface in the 2d and peak 16d, LSD’s low was 4d and peak 8d, the low of hippocampus PFC, S1Tr was 2d ,16d and peak 8d, the low of CA1, CA2, CA3, CA4 was 2d 24d and peak 8d, the low of the dentate gyrus, dentate gyrus under was 1d 24d,and peak 8d, PLCo’s low was in the 2d and peak 8d.(3) The number of microglias was increased post-injury and declined then, comparered with control, Septal PFC, S1FL, hippocampus PFC of PCC peak in 8d and 24d, CPu, LSV, LSD, the hippocampus Pir, CA1, CA2, CA3, CA4, the dentate gyrus, under the dentate gyrus, PLCo, flat pons, trapezoid body plane, olive tegmental area flat and the peak in the 8d, septal Pir, Tu, BST, S1Tr peak in the 16d, LD peak 1d and 16d. Septal PFC, S1FL, septal Pir, hippocampus PFC of MCC peak in 8d and 24d, Tu, Pir hippocampus peak in 16d, CPu, LSV, CA1, CA2, CA3, CA4, the dentate gyrus, under the dentate gyrus, LD, flat pons, trapezoid body plane, olive tegmental area flat and the peak in the 8d, LSD, BST peak at 1d and 8d, S1Tr peak at 1d and 24d, PLCo peak at 1d and 4d.Conclusion: (1) The number of pyknosis neurons in cerebral cortex was increased post-injury and declined then.(2) The number of macroglias was declined post-injury and increased then.(3) The number of microglias was increased post-injury and declined then更多还原