Objective To observe the changes of learning and memory ability in valproic caid (VPA) autism model rats and the expression of NF-κB positive neurons in hippocampal CA1 region after normal pressure and high oxygen intervention. Methods To animal model of autism was establishe by the methods of Schneider, the subjects of study were randomly divided into normal pressure high oxygen group and model control group, normal control group were randomly selected from only males offspring of Wistar rat were evaluatepregnancy by intraperitoneal injection of the same amount of normal saline (each group 12).The learning and memory of the autism model rats were evaluated by the Y electricity maze test after the normal pressure and high oxygen intervention.The immunohistochemistry methods and image analysis were used to examine the number of NF-κB positive neurons in hippocampal CA1 region in different groups. Results The trying times of the normal pressure high oxygen group after treatment was less than those before treatment (31.08±0.99 vs 31.67±0.89, t=2.887, P=0.015), the memory times was increased(3.02±0.67 vs 2.62±0.52, t=-2.379, P=0.036).The number of the NF-κB positive neurons of the model control group was more than that of the normal control group, with statistical differences between them(4.67±1.58 vs 3.00±1.54, t=2.639, P=0.015).The number of the NF-κB positive neurons of the normal pressure high oxygen group was less than that of the model control group, with statistical differences between them(3.17±1.27 vs 4.67±1.58, t=2.588, P=0.017). Conclusions The pathogenesis of autism may be related to the expression level of NF-κB in the hippocampal CA1 region .The intervention of normal pressure high oxygen can reduce the expression of NF-κB in the hippocampal CA1 region of VPA autism model rats and improve their learning and memory ability
Key words
autism /
normal pressure high oxygen /
learning and memory /
nuclear transcription factor kappa B /
rats
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References
[1] Lauritsen MB.Autism spectrum disorders[J].Eur Child Adolesc Psychiatry, 2013, 22(S2):37 -42.
[2] Bent S, Bertoglio K, Ashwood P, et al.Brief report:Hyperbaric oxygen therapy (HBOT) in children with autism spectrum disorder:a clinical trial[J].J Autism Dev Disord, 2012, 42(6):1127-1132.
[3] Bryńska A.Seeking the aetiology of autistic spectrum disorder.Part 2:Functional neuroimaging[J].Psychiatr Pol, 2012, 46(6):1061-1071.
[4] Yang WH, Jing J, Xiu LJ, et al.Regional cerebral blood flow in children with autism spectrum disorders:a quantitative99mTc-ECD brain SPECT study with statistical parametric mapping evaluation[J].Chin Med J (Engl), 2011, 124(9):1362-1366.
[5] Bellani M, Calderoni S, Muratori F, et al.Brain anatomy of autism spectrum disorders I.Focus on corpus callosum[J].Epidemiol Psychiatr Sci, 2013, 26(3):1-5.
[6] Ghanizadeh A.Nuclear factor kappa B may increase insight into the management of neuroinflammation and excitotoxicity in autism[J].Expert Opin Ther Targets, 2011, 15(6):781-783.
[7] Schneider T, Przewlocki R.Behavioral alterations in rats prenatally exposed to valproic acid:animal of autism[J].Neuropsychopharmacology, 2005, 30(1):80-89. [8] Kim KC, Kim P, Go HS, et al.Male-specific alteration in excitatory post-synaptic development and social interaction in pre-natal valproic acid exposure model of autism spectrum disorder[J].J Neurochem, 2013, 124(6):832-843.
[9] 张博爱, 张军艳, 朱红灿, 等.电迷宫训练对全脑缺血大鼠学习记忆能力的影响[J].郑州大学学报:医学版, 2008, 43(2):342-345.
[10] Andersen PN, Hovik KT, Skogli EW, et al.Symptoms of ADHD in children with high-functioning autism are related to impaired verbal working memory and verbal delayed recall[J].PLoS One, 2013, 8(5):e64842.
[11] Hu X, Zhang Y, Li W.Preconditioning with sevoflurane ameliorates spatial learning and memory deficit after focal cerebral ischemia-reperfusion in rats[J].Int J Dev Neurosci, 2013, 31(5):328-333.
[12] 陈晶, 陈燕惠.高压氧对缺氧缺血性脑损伤大鼠海马突触超微结构及突触素表达的影响[J].中华儿科杂志, 2010, 48(3):199-203.
[13] Garcia AJ 3rd, Putnam RW, Dean JB.Hyperbaric hyperoxia and normobaric reoxygenation increase excitability and activate oxygen-induced potentiation in CA1 hippocampal neurons[J].J Appl Physiol, 2010, 109(3):804-819.
[14] Bigdeli MR, Asheghabadi M, Khalili A.Time course of neuroprotection induced by normobaric hyperoxia in focal cerebral ischemia[J].Neurol Res, 2012, 34(5):439-446.
[15] 高宝兵, 龙志敏, 贺桂琼, 等.常压高氧处理对APP/PS1转基因小鼠空间学习记忆能力的影响[J].中华行为医学与脑科学杂志, 2009, 18(12):1064-1066.
[16] Bloch Y, Applebaum J, Osher Y, et al.Normobaric hyperoxia treatment of schizophrenia[J].J Clin Psychopharmacol, 2012, 32(4):525-530.
[17] Cheng O, Ostrowski RP, Liu W, et al.Activation of liver X receptor reduces global ischemic brain injury by reduction of nuclear factor-kappa B[J].Neuroscience, 2010, 166(4):1101-1109.
[18] Chen L, Wang L, Zhang X, et al.The protection by Octreotide against experimental ischemic stroke:up-regulated transcription factor Nrf2, HO-1 and down-regulated NF-kB expression[J].Brain Res, 2012, 26(9):80-87.
[19] 陈坤, 蒋朴, 徐颖, 等.Toll样受体4在新生小鼠常压高氧脑损伤中的作用[J].免疫学杂志, 2012, 28(2):98-103.
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