Hu Shou-Sen, Mei Ling, Chen Jian-Yong, Huang Zhi-Wu, Wu Hao
Department of Otolaryngology-Head and Neck Surgery, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, 1665 Kongjiang Road, Shanghai, 200092, China.
Ear Institute, Shanghai Jiao Tong University School of Medicine, 1665 Kongjiang Road, Shanghai, 200092, China.
Eur Arch Otorhinolaryngol. 2016 Feb;273(2):325-32. doi: 10.1007/s00405-014-3479-3. Epub 2015 Jan 31.
Spontaneous neuronal activity in dorsal cochlear nucleus (DCN) may be involved in the physiological processes underlying salicylate-induced tinnitus. As a neuronal activity marker, immediate-early gene (IEG) expression, especially activity-dependent cytoskeletal protein (Arc/Arg3.1) and the early growth response gene-1 (Egr-1), appears to be highly correlated with sensory-evoked neuronal activity. However, their relationships with tinnitus induced by salicylate have rarely been reported in the DCN. In this study, we assessed the effect of acute and chronic salicylate treatment on the expression of N-methyl D-aspartate receptor subunit 2B (NR2B), Arg3.1, and Egr-1. We also observed ultrastructural alterations in the DCN synapses in an animal model of tinnitus. Levels of mRNA and protein expression of NR2B and Arg3.1 were increased in rats that were chronically administered salicylate (200 mg/kg, twice daily for 3, 7, or 14 days). These levels returned to baseline 14 days after cessation of treatment. However, no significant changes were observed in Egr-1 gene expression in any groups. Furthermore, rats subjected to long-term salicylate administration showed more presynaptic vesicles, thicker and longer postsynaptic densities, and increased synaptic interface curvature. Alterations of Arg3.1 and NR2B may be responsible for the changes in the synaptic ultrastructure. These changes confirm that salicylate can cause neural plasticity changes at the DCN level.
耳蜗背侧核(DCN)的自发性神经元活动可能参与了水杨酸盐诱导耳鸣的生理过程。作为一种神经元活动标记物,即刻早期基因(IEG)表达,尤其是活动依赖性细胞骨架蛋白(Arc/Arg3.1)和早期生长反应基因-1(Egr-1),似乎与感觉诱发的神经元活动高度相关。然而,在DCN中,它们与水杨酸盐诱导的耳鸣之间的关系鲜有报道。在本研究中,我们评估了急性和慢性水杨酸盐处理对N-甲基-D-天冬氨酸受体亚基2B(NR2B)、Arg3.1和Egr-1表达的影响。我们还在耳鸣动物模型中观察了DCN突触的超微结构改变。长期给予水杨酸盐(200mg/kg,每日两次,共3、7或14天)的大鼠中,NR2B和Arg3.1的mRNA和蛋白表达水平升高。在停药14天后,这些水平恢复到基线。然而,在任何组中均未观察到Egr-1基因表达的显著变化。此外,长期给予水杨酸盐的大鼠显示出更多的突触前囊泡、更厚更长的突触后致密物以及增加的突触界面曲率。Arg3.1和NR2B的改变可能是突触超微结构变化的原因。这些变化证实水杨酸盐可在DCN水平引起神经可塑性改变。