Lee Jin-Koo, Maskey Dhiraj, Kim Myeung Ju
Department of Pharmacology, Dankook University College of Medicine, Cheonan, South Korea.
Cells Tissues Organs. 2017;204(5-6):304-313. doi: 10.1159/000479961. Epub 2017 Nov 4.
The circling mouse serves as a hearing loss model. It has spontaneous tmie gene mutations that cause hair cell and cochlear degeneration. However, little is known about the role of the tmie gene in superior olivary complex (SOC) regions, in which sound information from the two ears is integrated and primarily relayed to the nuclei of the lateral lemniscus and inferior colliculus. Several studies have reported that abnormal calcium (Ca2+) homeostasis is associated with the pathology of hearing loss. This study investigated the distribution of Ca2+-binding proteins (CaBPs), such as calbindin D28k, parvalbumin, and calretinin, in the SOC of the circling mouse on postnatal day 16. A comparison of wild-type (+/+), heterozygous (+/cir), and homozygous (cir/cir) mice showed that CaBP immunoreactivity was significantly decreased in the auditory nucleus of the SOC of homozygous (cir/cir) mice. A decline in the CaBPs level in the SOC may be the result of hearing loss through hair cell and cochlear degeneration following tmie gene mutation.
转圈小鼠可作为听力损失模型。它存在自发性tmie基因突变,会导致毛细胞和耳蜗退化。然而,关于tmie基因在橄榄上核复合体(SOC)区域中的作用却知之甚少,在该区域,来自双耳的声音信息被整合并主要传递至外侧丘系核和下丘核。多项研究报告称,异常的钙(Ca2+)稳态与听力损失的病理过程相关。本研究调查了出生后第16天的转圈小鼠的SOC中钙结合蛋白(CaBP)(如钙结合蛋白D28k、小白蛋白和钙视网膜蛋白)的分布情况。对野生型(+/+)、杂合子(+/cir)和纯合子(cir/cir)小鼠的比较显示,纯合子(cir/cir)小鼠的SOC听觉核中CaBP免疫反应性显著降低。SOC中CaBP水平的下降可能是tmie基因突变后毛细胞和耳蜗退化导致听力损失的结果。