水杨酸钠注射后大鼠听觉通路突触素表达的变化

目的：检测水杨酸钠注射后大鼠耳蜗核、上橄榄核、下丘脑及听皮层突触素表达的变化，探讨听觉通路的可塑性变化与耳鸣发病机制的关系。方法将36只大鼠随机分为6组（每组6只）：按照注射药物时间长短的不同分为Ⅰ、Ⅱ组，其中Ⅰ组注射药物时间为14d，Ⅱ组注射药物时间为21d（空白对照组不注射药物）；两组又各自分为A、B、C 3个亚组，其中A组为水杨酸钠组，B为0.9%氯化钠溶液组，C为空白对照组。ⅠA组：每次条件反射训练前3h腹腔注射10%水杨酸钠溶液（350mg/kg），至实验结束；ⅠB组：每次条件反射训练前3h腹腔注射同体积0.9%氯化钠溶液，至实验结束；ⅠC组：饲养在安静环境中，不限饮食，不注射药物，不进行条件反射训练；ⅡA、ⅡB、ⅡC组的分组方法同前。应用免疫组化技术检测各组大鼠听觉通路中4个核团突触素表达的情况。结果早期耳鸣组（ⅠA）与持续耳鸣组（ⅡA）同其余组大鼠相比，耳蜗核、上橄榄核、下丘脑、听皮层突触素的表达都明显增多（均P＜0.01）；且ⅡA组各核团中突触素的表达均较ⅠA组增多（均P＜0.01）。结论水杨酸钠注射可成功建立大鼠耳鸣模型，耳鸣大鼠听觉通路突触素表达的改变为耳鸣的中枢源性学说提供了部分理论依据。

Expression of snaptophysin in rat auditory pathway after sodium salicylate injection

Objective To investigate the expression of synaptophysin in cochlear nucleus, superior olivary nucleus, infe-rior col iculus and auditory cortex of rats after salicylate injection. Methods Thirty- six Wistar rats were randomly divided into 3 groups： rats in group A received intraperitoneal （i.p） infection of 350 mg/kg sodium salicylate 3h before conditioned response training, while rats in group B received i.p injection of normal saline 3h before conditioned response training, and no conditioned response training and drug injection was given to animals in group C （blank control）;the animals were further divided into 6 sub-groups （n=6, in each subgroup）：AI, BI and CI subgroups received treatment for 7d, subgroups AII, BII and CII for 14d. Sam-ples were col ected after animals were sacrificed, the expression of synaptophysin in rat cochlear nucleus, superior olivary nu-cleus, inferior col iculus and auditory cortex were detected by immunohistochemical technique. Results The expressions of synaptophysin in cochlear nucleus, superior olivary nucleus, hypothalamus and auditory cortex in group A were significantly higher than those in groups B and C （P〈0.01） , and the expression of synaptophysin inⅡA group was higher than that inⅠA group in auditory pathway tested （P〈0.01）. Conclusion The tinnius model can be established by injection of sodium salicylate in rats, and the alteration of synaptophysin expression in auditory nucleus provides a experimental basis for the central source of tinnius.