| Background and objective: Concussive brain injury (CBI), seen frequently in traffic accidents and criminal cases, has been reported to be predominating in human traumatic brain injury (TBI) and be characterized by both a transient loss of consciousness in the absence of localized gross anatomical changes in the brain and a post-concussion syndrome including long-lasting cognitive deficits. In human CBI, learning and memory deficits are those of the most persistent disabilities, to which not enough attention has been given, however, and systematic study is needed. Most of CBI cases are involved with lawsuit, lacking of objective evidences, forensic medicine identification of CBI remains difficult. The neural mechanisms of learning and memory deficits following CBI not being established, diagnosis and treatment for CBI remains difficult also. Therefore, it is important and necessary to duplicate the animal model of concussive brain injury, and make a systematic study on the neural mechanisms of learning and memory deficits following CBI.Materials and methods: 84 SD rats (male 40 and female 44) were randomly divided into 10 groups. Animals in group A (n=10), group C (n=10), group E(n=10), group G(n=10), group I(n=10) and group J(n=10) were assigned to receive a concussive brain injury, animals in group B(n=6), group D(n=6), group F(n=6) and group H(n=6) were assigned to receive a sham injury, respectively. To investigate the retrograde amnesia seen frequently in human CBI, animals in group A and in group B were trained in Morris water maze pre-concussion (sham injury in group B), and theirspatial memory abilities were tested P<0st-concussion. To investigate the learning and memory deficits following CBI in rats, rats in group C and in group D were used to test spatial learning, reference memory and working memory abilities P<0st-concussion.To detect the neural mechanisms of learning and memory deficits following CBI, rats in group E and in group F were assigned to sacrifice on day 3 P<0st-concussion to detect whether an aP<0ptosis mechanism was included in the hipP<0campus CA3 pyramidal cells damages. Rats in group G, in group h, in group I and in group J were assigned to receive injury/NS treatment, sham injury/NS treatment, injury/naloxone hydrochloride treatment, and injury/sulpiride treatment, respectively. Learning and memory abilities were tested following injury/treatment, then rats were sacrificed on day!4 P<0st-concussion, the level of intracellular calcium in hipP<0campus pyramidal cells was measured employing the technique of laser confocal scanning microscope, numbers of pyramidal cells in CA3 area were counted with Nissl staining.Results:1 .The number of crossing the former site of the hidden platform was tested 24h, 48h, 72h P<0st-concussion, respectively. The number in rats of group A was reduced significantly compared to that in rats of group B, when tested 24h P<0st-concussion (P<0.05) . While no statistical difference was found when tested 48h and 72h P<0st-concussion (P>0.05) . The results suggested a transient retrograde amnesia happened following CBI in rats.2.Escape latencies in rats of group C and group D were tested day8-13 P<0st-concussion. The mean escape latencies in rats of group C was increased significantly compared to that in rats of group D each day (P<0.05) . The mean number of crossing the former site of the hidden platform in rats of group C was reduced significantly compared to that in rats of group D tested on day 13 P<0st-concussion (P<0.05) . T-test showed a damage effect of CBI on the spatiallearning and memory (reference memory) in rats. Working memory deficits were also observed in CBI rats on day 15-18 P<0st-concussion.3.one-way ANOVA showed a protective effect of naloxone and sulpiride on learning and memory deficits following CBI in rats. The escape latencies in rats of group I and group J were significantly reduced compared to those in rats of group G (P<0.05) . The mean number of crossing the former site of the hidden platform in rats of g...
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