摘要
目的通过建立听觉剥夺(auditory deprivation,AD)的动物模型,探讨脑源性神经生长因子(brain-derived neurotrophic factor,BDNF)和其功能性受体酪氨酸激酶B(tropomyosin receptor kinase B,TrkB)与听皮层可塑性的关系。方法 48只SD大鼠随机分为实验组和对照组,每组24只,采用耳后切口暴露听泡并打开,实验组行双侧耳蜗损毁术建立大鼠AD模型,对照组不损毁耳蜗。于术后2w分别检测两组动物ABR反应阈,并应用实时荧光定量PCR技术和免疫组织化学方法,于术后2、4、6、8w测定两组大鼠听皮层BDNF和TrkB基因mRNA和蛋白表达水平。结果术后2w,实验组动物双耳ABR反应阈明显高于对照组(P<0.05);听觉剥夺后,听皮层BDNF与TrkB有相同的表达变化趋势,除术后6w外,实验组第2、8wBDNF与TrkB基因mRNA和蛋白表达量低于对照组(P<0.05),而第4w二者的表达量高于对照组(P<0.05)。结论 BDNF通过与功能性受体TrkB结合,参与听皮层神经元可塑性的调节,可能对神经元的损害具有代偿性修复作用。
Objective To investigate the relationship between brain-derived neurotrophic factor（BDNF）and tropomyosin receptor kinase B（TrkB）and the plasticity of auditory cortex（AC）in auditory deprivation（AD）fo animal model.Methods Forty-eight SD rats were randomly divised into 2groups（24rats/group）.Experiment group received bilateral cochlear ablation while control group did not.AD model was established by bilateral cochlear ablation through retroauricular incision.Technology of real-time polymerase chain reaction（RT-PCR）and immunohistochemistry method were used to observe the expressions of BDNF and TrkB in AC at 2wks,4wks,6wks and 8wks after operation.Statistical analysis was conducted with SPSS 13.0software.Results Bilateral cochlear ablation resulted in serious hearing loss and the threshold of ABR was significantly increased（P0.05）.The expression patterns of BDNF and TrkB in auditory cortex were similar with each other after auditory deprivation,which decreased at 2wks,increased and peaked at 4wks,and then decreased afterward.The difference between each AD group and control group was statistically significant（P0.05）except for 6wks.Conclusion BDNF participates in the plasticity change of auditory cortex through BDNF-TrkB signal passway which may play critical roles in the impairment of neuron.
出处
《听力学及言语疾病杂志》
CAS
CSCD
北大核心
2013年第4期379-382,共4页
Journal of Audiology and Speech Pathology
基金
河北省自然科学基金(C2011206036)
河北省卫生厅医学科学研究重点课题计划(20110375)资助
关键词
听觉剥夺
脑源性神经生长因子
酪氨基激酶B
可塑性
听皮层
Auditory deprivation
Brain-derived neurotrophic factor
Tropomyosin receptor kinase B
Plasticity
Auditory cortex
