Caragli Valeria, Di Pasquale Fiasca Valerio M, Genovese Elisabetta, Martini Alessandro
Otorhinolaryngology-Head and Neck Surgery, Audiology Program, University of Modena and Reggio Emilia, 41125 Modena, Italy.
Section of Otorhinolaryngology-Head and Neck Surgery, Department of Neurosciences, University of Padua, 35128 Padua, Italy.
Audiol Res. 2025 Jun 23;15(4):75. doi: 10.3390/audiolres15040075.
: Kölliker's organ (KO), a transient structure in the cochlea, plays a critical role in the auditory maturation of mammals, particularly during embryonic and early postnatal development. This organ is essential for the proper differentiation and function of cochlear cells, acting as a pivotal source of signalling molecules that influence hair cell development and synaptic connectivity. : This study systematically analyses the literature according to the PRISMA statement in order to evaluate the function roles of KO during cochlea development, reporting the molecular mechanisms and signalling pathways involved. : From our study, it emerged that KO supporting cells release adenosine triphosphate (ATP) through connexin hemichannels, initiating a cascade of intracellular calcium (Ca) signalling in adjacent inner hair cells (IHCs). This signalling promotes the release of glutamate, facilitating synaptic excitation of afferent nerve fibres and enhancing auditory neuron maturation prior to the onset of hearing. Additionally, the spontaneous electrical activity generated within KO supports the establishment of essential neural connections in the auditory pathway. The dynamic interplay between ATP release, Ca signalling, and morphological changes in KO is crucial for cochlear compartmentalisation and fluid regulation, contributing to the formation of endolymph and perilymph. Furthermore, KO supports cellular plasticity and may provide a reservoir of precursor cells capable of trans-differentiating into hair cells under specific conditions. : Dysregulation of KO function or delayed degeneration of its supporting cells has been implicated in auditory disorders, underscoring the importance of this organ in normal cochlear development and auditory function. Despite its identification over a century ago, further investigation is necessary to elucidate the molecular mechanisms underlying KO's contributions to auditory maturation, particularly in human physiology.
科利克器(KO)是耳蜗中的一种短暂结构,在哺乳动物的听觉成熟过程中起着关键作用,尤其是在胚胎期和出生后早期发育阶段。该器官对于耳蜗细胞的正常分化和功能至关重要,它是影响毛细胞发育和突触连接的信号分子的关键来源。本研究根据PRISMA声明系统地分析了文献,以评估KO在耳蜗发育过程中的功能作用,报告所涉及的分子机制和信号通路。从我们的研究中发现,KO支持细胞通过连接蛋白半通道释放三磷酸腺苷(ATP),在相邻的内毛细胞(IHC)中引发细胞内钙(Ca)信号级联反应。这种信号传导促进谷氨酸的释放,促进传入神经纤维的突触兴奋,并在听力开始前增强听觉神经元的成熟。此外,KO内产生的自发电活动支持听觉通路中基本神经连接的建立。ATP释放、Ca信号传导和KO形态变化之间的动态相互作用对于耳蜗的分隔和液体调节至关重要,有助于内淋巴和外淋巴的形成。此外,KO支持细胞可塑性,并可能提供在特定条件下能够转分化为毛细胞的前体细胞库。KO功能失调或其支持细胞的延迟退化与听觉障碍有关,这突出了该器官在正常耳蜗发育和听觉功能中的重要性。尽管它在一个多世纪前就已被发现,但仍有必要进一步研究以阐明KO对听觉成熟贡献的分子机制,特别是在人类生理学方面。