Lee Jin-Koo, Kim Myeung Ju
Department of Pharmacology, Dankook University College of Medicine, Cheonan, Korea.
Department of Anatomy, Dankook University College of Medicine, Cheonan, Korea.
Anat Cell Biol. 2017 Sep;50(3):230-238. doi: 10.5115/acb.2017.50.3.230. Epub 2017 Sep 20.
The circling mice with gene mutation are known as an animal deafness model, which showed hyperactive circling movement. Recently, the reinvestigation of circling mouse was performed to check the inner ear pathology as a main lesion of early hearing loss. In this trial, the inner ear organs were not so damaged to cause the hearing deficit of circling (cir/cir) mouse at 18 postnatal day (P18) though auditory brainstem response data indicated hearing loss of cir/cir mice at P18. Thus, another mechanism may be correlated with the early hearing loss of cir/cir mice at P18. Hearing loss in the early life can disrupt the ascending and descending information to inferior colliculus (IC) as integration site. There were many reports that hearing loss could result in the changes in Ca concentration by either cochlear ablation or genetic defect. However, little was known to be reported about the correlation between the pathology of IC and Ca changes in circling mice. Therefore, the present study investigated the distribution of calcium-binding proteins (CaBPs), calbindin-D28k, parvalbumin, and calretinin immunoreactivity (IR) in the IC to compare among wild-type (+/+), heterozygous (+/cir), and homozygous (cir/cir) mice by immunohistochemistry. The decreases of CaBPs IR in cir/cir were statistically significant in the neurons as well as neuropil of IC. Thus, this study proposed overall distributional alteration of CaBPs IR in the IC caused by early hearing defect and might be helpful to elucidate the pathology of central auditory disorder related with Ca metabolism.
具有基因突变的转圈小鼠被认为是一种动物耳聋模型，其表现出过度活跃的转圈运动。最近，对转圈小鼠进行了重新研究，以检查内耳病理学情况，将其作为早期听力损失的主要病变。在该试验中，尽管听性脑干反应数据表明18日龄（P18）的cir/cir小鼠存在听力损失，但内耳器官并未严重受损到导致其听力缺陷。因此，可能存在另一种机制与P18时cir/cir小鼠的早期听力损失相关。早期生活中的听力损失会扰乱作为整合位点的下丘（IC）的上下行信息。有许多报道称，听力损失可通过耳蜗切除或基因缺陷导致钙浓度变化。然而，关于转圈小鼠中IC病理学与钙变化之间的相关性，鲜少有报道。因此，本研究通过免疫组织化学研究了钙结合蛋白（CaBPs）、钙结合蛋白-D28k、小白蛋白和钙视网膜蛋白免疫反应性（IR）在IC中的分布，以比较野生型（+/+）、杂合子（+/cir）和纯合子（cir/cir）小鼠。cir/cir小鼠中CaBPs IR的降低在IC的神经元以及神经毡中具有统计学意义。因此，本研究提出早期听力缺陷导致IC中CaBPs IR的整体分布改变，这可能有助于阐明与钙代谢相关的中枢听觉障碍的病理学。
