摘要
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 investigate the hypothesis that the central nervous system is involved in tinnims by testing immediately early gene Arc/arg3.1 in the auditory brainstem. Methods Forty-eight Wistar rats were randomly divided into 6 groups ( n = 8 in each group) : During establishing a conditioned response, groups Ⅰ and Ⅳ received a single intraperitoneally injected ( i. p. ) dose of 400 nag sodium salicylate per kg bodyweight dissolved in physiological saline 2 hours before training, while groups Ⅱ and Ⅴ were injected i.p. with the same dose of physiological saline. Undisturbed controls were groups Ⅲ and Ⅵ. After group Ⅳ maneged to establish a model of tinnitus, these rats continued to receive injections of the same dose of sodium salicylate for ten days. Groups Ⅰ , Ⅱ and Ⅲ were sacrificed and samples were harvested together; groups Ⅳ, Ⅴ and Ⅵ were sacrificed and were harvested together samples together. Then SYBR Greenl real-time relative quantitative RT-PCR was used to detect expression of gene ARC/arg3.1 in these three auditory nuclei. Results Expresseion levels of Arc mRNA in the cochlear nucleus first down-regulated ( P 〈 0.05 ) then climbed back slightly ( P 〈 0.05 ) ; Arc mRNA of the inferior colliculus increased and maintained a high degree, but no longer climbed( P 〈 0.01 ) ; finally, we failed to find any change in nuclei olivaris superior( P 〉 0.05 ). Conclusions The alteration of the Arc mRNA in the auditory brainstem further supports tinnitus-related plasticity in the auditory center.
出处
《山东大学耳鼻喉眼学报》
CAS
2010年第1期21-24,共4页
Journal of Otolaryngology and Ophthalmology of Shandong University
基金
厦门市科技局资助项目(编号3502Z20064017)