The upregulation of K+ and HCN channels in developing spiral ganglion neurons is mediated by cochlear inner hair cells
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View abstract on PubMed
Summary
This summary is machine-generated.Spontaneous activity from inner hair cells (IHCs) is crucial for the maturation of spiral ganglion neurons (SGNs). Otoferlin deficiency in IHCs impairs K+ channel expression in SGNs, leading to hyperexcitability and delayed SGN development.
Area Of Science
- Neuroscience
- Auditory Neuroscience
- Developmental Neuroscience
Background
- Spiral ganglion neurons (SGNs) transmit auditory information from inner hair cells (IHCs) to the brain.
- SGNs exhibit diverse response properties for encoding sound intensity.
- Spontaneous activity in IHCs during development is thought to shape SGN characteristics, but its role is unclear.
Purpose Of The Study
- To investigate the role of spontaneous inner hair cell (IHC) activity in the maturation of spiral ganglion neurons (SGNs).
- To determine the impact of otoferlin deficiency on SGN biophysical properties and gene expression.
Main Methods
- Utilized otoferlin knockout (Otof-/-) mice to eliminate Ca2+-dependent exocytosis in IHCs.
- Performed electrophysiological recordings to assess SGN firing characteristics and ion channel expression.
- Conducted RNA-sequencing to analyze gene expression changes in SGNs.
Main Results
- Developing SGNs in Otof-/- mice showed delayed maturation, failing to upregulate key ion channels (Kv, HCN).
- Absence of IHC spontaneous activity resulted in hyperexcitable SGNs with immature firing properties.
- Identified a novel biophysical marker (resurgent K+ current) in SGNs synapsing with the pillar side of IHCs.
- RNA-sequencing revealed downregulation of several potassium channels in SGNs lacking IHC activity.
Conclusions
- Spontaneous Ca2+-dependent activity in pre-hearing IHCs is essential for regulating key biophysical and molecular features of developing SGNs.
- Otoferlin-mediated IHC exocytosis is critical for the functional maturation of type I SGNs.
- Disruption of IHC activity leads to SGN hyperexcitability and impaired auditory development.
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