| [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... |
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