Dayaratne M W Nishani, Vlajkovic Srdjan M, Lipski Janusz, Thorne Peter R
Department of Physiology, Faculty of Medical and Health Sciences, The University of Auckland, Private Bag 92019, Auckland 1142, New Zealand ; Centre for Brain Research, Faculty of Medical and Health Sciences, The University of Auckland, Private Bag 92019, Auckland 1142, New Zealand.
Department of Physiology, Faculty of Medical and Health Sciences, The University of Auckland, Private Bag 92019, Auckland 1142, New Zealand ; Centre for Brain Research, Faculty of Medical and Health Sciences, The University of Auckland, Private Bag 92019, Auckland 1142, New Zealand ; Section of Audiology, Faculty of Medical and Health Sciences, The University of Auckland, Private Bag 92019, Auckland 1142, New Zealand.
Biomed Res Int. 2014;2014:367939. doi: 10.1155/2014/367939. Epub 2014 Aug 20.
Prior to the "onset of hearing," developing cochlear inner hair cells (IHCs) and primary auditory neurons undergo experience-independent activity, which is thought to be important in retaining and refining neural connections in the absence of sound. One of the major hypotheses regarding the origin of such activity involves a group of columnar epithelial supporting cells forming Kölliker's organ, which is only present during this critical period of auditory development. There is strong evidence for a purinergic signalling mechanism underlying such activity. ATP released through connexin hemichannels may activate P2 purinergic receptors in both Kölliker's organ and the adjacent IHCs, leading to generation of electrical activity throughout the auditory system. However, recent work has suggested an alternative origin, by demonstrating the ability of IHCs to generate this spontaneous activity without activation by ATP. Regardless, developmental abnormalities of Kölliker's organ may lead to congenital hearing loss, considering that mutations in ion channels (hemichannels, gap junctions, and calcium channels) involved in Kölliker's organ activity share strong links with such types of deafness.
在“听力开始”之前,发育中的耳蜗内毛细胞(IHC)和初级听觉神经元会经历与经验无关的活动,这种活动被认为在无声环境下保留和完善神经连接方面很重要。关于这种活动起源的主要假设之一涉及一群形成柯蒂氏器的柱状上皮支持细胞,柯蒂氏器仅在听觉发育的这个关键时期存在。有强有力的证据表明这种活动存在嘌呤能信号传导机制。通过连接蛋白半通道释放的ATP可能会激活柯蒂氏器和相邻内毛细胞中的P2嘌呤能受体,从而导致整个听觉系统产生电活动。然而,最近的研究通过证明内毛细胞在没有ATP激活的情况下产生这种自发活动的能力,提出了另一种起源。无论如何,考虑到参与柯蒂氏器活动的离子通道(半通道、缝隙连接和钙通道)中的突变与这类耳聋有密切联系,柯蒂氏器的发育异常可能导致先天性听力损失。