scholarly journals Kölliker’s Organ and the Development of Spontaneous Activity in the Auditory System: Implications for Hearing Dysfunction

2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
M. W. Nishani Dayaratne ◽  
Srdjan M. Vlajkovic ◽  
Janusz Lipski ◽  
Peter R. Thorne
Keyword(s):  
Spontaneous Activity ◽  
Auditory System ◽  
Purinergic Signalling ◽  
Auditory Neurons ◽  
Supporting Cells ◽  
Developmental Abnormalities ◽  
Neural Connections ◽  
P2 Purinergic Receptors ◽  
Auditory Development ◽  
Connexin Hemichannels

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.

scholarly journals Purinergic signaling controls spontaneous activity in the auditory system throughout early development

2020 ◽  
Author(s):  
Travis A. Babola ◽  
Sally Li ◽  
Zhirong Wang ◽  
Calvin Kersbergen ◽  
Ana Belén Elgoyhen ◽  
...  
Keyword(s):  
Electrical Activity ◽  
Spontaneous Activity ◽  
Auditory System ◽  
Developmental Disorders ◽  
Developmental Stages ◽  
Purinergic Signaling ◽  
Atp Release ◽  
Auditory Neurons ◽  
Ganglion Neurons

ABSTRACTSpontaneous bursts of electrical activity in the developing auditory system arise within the cochlea prior to hearing onset and propagate through future sound processing circuits of the brain to promote maturation of auditory neurons. Studies in isolated cochleae revealed that this intrinsically generated activity is initiated by ATP release from inner supporting cells (ISCs), resulting in activation of purinergic autoreceptors, K+ efflux and subsequent depolarization of inner hair cells (IHCs). However, little is known about when this activity emerges or whether different mechanisms underlie distinct stages of development. Here we show that spontaneous electrical activity in mouse cochlea emerges within ISCs during the late embryonic period, preceding the onset of spontaneous correlated activity in IHCs and spiral ganglion neurons (SGNs), which begins at birth and follows a base to apex developmental gradient. At all developmental stages, pharmacological inhibition of P2Y1 metabotropic purinergic receptors dramatically reduced spontaneous activity in these three cell types. Moreover, in vivo imaging within the inferior colliculus of awake mice revealed that auditory neurons within future isofrequency zones exhibit coordinated neural activity at birth. The frequency of these discrete bursts increased progressively during the postnatal prehearing period, yet remained dependent on P2RY1. Analysis of mice with disrupted cholinergic signaling in the cochlea, indicate that this input modulates, rather than initiates, spontaneous activity before hearing onset. Thus, the auditory system uses a consistent mechanism involving ATP release from ISCs and activation of purinergic autoreceptors to elicit coordinated excitation of neurons that will process similar frequencies of sound.SIGNIFICANCE STATEMENTIn developing sensory systems, groups of neurons that will process information from similar sensory space exhibit highly correlated electrical activity that is critical for proper maturation and circuit refinement. Defining the period when this activity is present, the mechanisms responsible and the features of this activity are crucial for understanding how spontaneous activity influences circuit development. We show that, from birth to hearing onset, the auditory system relies on a consistent mechanism to elicit correlate firing of neurons that will process similar frequencies of sound. Targeted disruption of this activity will increase our understanding of how these early circuits mature and may provide insight into processes responsible for developmental disorders of the auditory system.

scholarly journals Efferent feedback enforces bilateral coupling of spontaneous activity in the developing auditory system

2020 ◽  
Author(s):  
Yixiang Wang ◽  
Maya Sanghvi ◽  
Alexandra Gribizis ◽  
Yueyi Zhang ◽  
Lei Song ◽  
...  
Keyword(s):  
Spontaneous Activity ◽  
Auditory System ◽  
Activity Patterns ◽  
Descending Pathways ◽  
Efferent System ◽  
Cholinergic Pathway ◽  
The Central Nervous System ◽  
Necessary And Sufficient ◽  
Circuit Formation

SummaryIn the developing auditory system, spontaneous activity generated in the cochleae propagates into the central nervous system to promote circuit formation before hearing onset. Effects of the evolving peripheral firing pattern on spontaneous activity in the central auditory system are not well understood. Here, we describe the wide-spread bilateral coupling of spontaneous activity that coincides with the period of transient efferent modulation of inner hair cells from the medial olivochlear (MOC) system. Knocking out the α9/α10 nicotinic acetylcholine receptor, a requisite part of the efferent cholinergic pathway, abolishes these bilateral correlations. Pharmacological and chemogenetic experiments confirm that the MOC system is necessary and sufficient to produce the bilateral coupling. Moreover, auditory sensitivity at hearing onset is reduced in the absence of pre-hearing efferent modulation. Together, our results demonstrate how ascending and descending pathways collectively shape spontaneous activity patterns in the auditory system and reveal the essential role of the MOC efferent system in linking otherwise independent streams of bilateral spontaneous activity during the prehearing period.

scholarly journals Spontaneous activity in the developing auditory system

2014 ◽  
Vol 361 (1) ◽  
pp. 65-75 ◽  
Author(s):  
Han Chin Wang ◽  
Dwight E. Bergles
Keyword(s):  
Spontaneous Activity ◽  
Auditory System

scholarly journals Homeostatic Control of Spontaneous Activity in the Developing Auditory System

Neuron ◽  
2018 ◽  
Vol 99 (3) ◽  
pp. 511-524.e5 ◽  
Author(s):  
Travis A. Babola ◽  
Sally Li ◽  
Alexandra Gribizis ◽  
Brian J. Lee ◽  
John B. Issa ◽  
...  
Keyword(s):  
Spontaneous Activity ◽  
Auditory System ◽  
Homeostatic Control

The origin of spontaneous activity in the developing auditory system

Nature ◽  
2007 ◽  
Vol 450 (7166) ◽  
pp. 50-55 ◽  
Author(s):  
Nicolas X. Tritsch ◽  
Eunyoung Yi ◽  
Jonathan E. Gale ◽  
Elisabeth Glowatzki ◽  
Dwight E. Bergles
Keyword(s):  
Spontaneous Activity ◽  
Auditory System

scholarly journals Physiological basis of noise-induced hearing loss in a tympanal ear

2019 ◽  
Author(s):  
Ben Warren ◽  
Georgina E Fenton ◽  
Elizabeth Klenschi ◽  
James FC Windmill ◽  
Andrew S French
Keyword(s):  
Hearing Loss ◽  
Ion Channels ◽  
Noise Exposure ◽  
Noise Induced Hearing Loss ◽  
Auditory Neurons ◽  
Supporting Cells ◽  
Physiological Basis ◽  
Positive Ions ◽  
Induced Changes ◽  
Stimulation Of

AbstractAcoustic overexposure, such as listening to music too loud and too often, results in noise-induced hearing loss. The pathologies of this prevalent sensory disorder begin in the synapses of the primary auditory receptors, their postsynaptic partners and supporting cells. The extent of noise-induced damage, however, is determined by over-stimulation of primary auditory receptors. When over-stimulated, an excessive amount of positive ions flood into the primary auditory receptors, triggering the activation of ion channels and possibly disrupting their ability to encode sound. A systematic characterisation of the electrophysiological function of primary auditory receptors is warranted to understand how noise-exposure impacts on downstream targets, where the pathologies of hearing loss begin. Here, we used the experimentally-accessible locust ear to characterise noise-induced changes in the auditory receptors. Although, we found a decrease in ability of the primary auditory neurons to encode sound, this is probably due to pathologies of their supporting cells.

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