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目的通过检测耳鸣大鼠听觉脑干中Arc/arg3.1的表达情况,以探讨耳鸣发生的中枢源性机制。方法将48只大鼠随机平均分为6组:Ⅰ组与Ⅳ组为水杨酸钠组,其中Ⅳ组大鼠在耳鸣模型建立成功后,继续每天同一时间腹腔注射相同剂量水杨酸钠溶液10d;Ⅱ、Ⅴ组为生理盐水对照组;Ⅲ、Ⅵ组为空白对照组。Ⅰ、Ⅱ、Ⅲ组在造模成功后同时断头取标本,而Ⅴ、Ⅵ组与Ⅳ组一起断头取标本。再利用实时荧光(sybgreenⅠ染料法)相对定量PCR检测Arc/arg3.1mRNA在听觉脑干3个核团中的表达情况。结果耳鸣大鼠Arc/arg3.1基因的表达水平在耳蜗核中先下降(P<0.05),而后又轻微回升(P<0.05);在下丘中表达水平上升到一定程度不再继续上升而维持在一定的较高的表达水平(P<0.01);上橄榄核中ArcmRNA未发现明显改变(P>0.05)。结论实验中耳鸣大鼠Arc/arg3.1表达水平的改变证实听觉脑干神经元发生了可塑性改变。
Objective To explore the central mechanism of tinnitus by detecting the expression of Arc / arg3.1 in the auditory brainstem of tinnitus rats. Methods Forty-eight rats were randomly divided into 6 groups randomly: group Ⅰ and group Ⅳ were sodium salicylate group. After successful establishment of the tinnitus model in group Ⅳ, the same dose of sodium salicylate solution 10d; group Ⅱ and group Ⅴ were normal saline control group; group Ⅲ and Ⅵ were blank control group. The specimens of Ⅰ, Ⅱ and Ⅲ were decapitated at the same time after successful modeling, while the specimens of Ⅴ, Ⅵ and Ⅳ were decapitated. Real-time fluorescence (sybgreenⅠ dye method) relative quantitative PCR was used to detect the expression of Arc / arg3.1mRNA in the three nuclei of auditory brainstem. Results The expression of Arc / arg3.1 gene in tinnitus rats decreased first (P <0.05) and then slightly increased in the cochlear nucleus (P <0.05). In the inferior colliculus, the expression level of Arc / arg3.1 increased to a certain extent and continued to rise At a certain higher level (P <0.01), ArcmRNA in the upper olivary nuclei did not change significantly (P> 0.05). Conclusion The change of Arc / arg3.1 expression in tinnitus rats during the experiment confirms the change of plasticity of auditory brainstem neurons.