scholarly journals Acoustic sensitivity and frequency selectivity of the guinea pig inner ear after total destruction of cochlear hair cells

1981 ◽  
Vol 70 (S1) ◽  
pp. S27-S27 ◽  
Author(s):  
Y. Cazals ◽  
J.‐M. Aran ◽  
J.‐P. Erre ◽  
A. Guilhaume
2018 ◽  
Vol 9 (9) ◽  
Author(s):  
Minjin Jeong ◽  
Molly O’Reilly ◽  
Nerissa K. Kirkwood ◽  
Jumana Al-Aama ◽  
Majlinda Lako ◽  
...  

2020 ◽  
Vol 21 (22) ◽  
pp. 8649
Author(s):  
Xin Deng ◽  
Zhengqing Hu

Regeneration of auditory hair cells in adult mammals is challenging. It is also difficult to track the sources of regenerated hair cells, especially in vivo. Previous paper found newly generated hair cells in deafened mouse by injecting a DNA methyltransferase inhibitor 5-azacytidine into the inner ear. This paper aims to investigate the cell sources of new hair cells. Transgenic mice with enhanced green fluorescent protein (EGFP) expression controlled by the Sox2 gene were used in the study. A combination of kanamycin and furosemide was applied to deafen adult mice, which received 4 mM 5-azacytidine injection into the inner ear three days later. Mice were followed for 3, 5, 7 and 14 days after surgery to track hair cell regeneration. Immunostaining of Myosin VIIa and EGFP signals were used to track the fate of Sox2-expressing supporting cells. The results show that (i) expression of EGFP in the transgenic mice colocalized the supporting cells in the organ of Corti, and (ii) the cell source of regenerated hair cells following 5-azacytidine treatment may be supporting cells during 5–7 days post 5-azacytidine injection. In conclusion, 5-azacytidine may promote the conversion of supporting cells to hair cells in chemically deafened adult mice.


1998 ◽  
Vol 255 (3) ◽  
pp. 127-131 ◽  
Author(s):  
T. Nakagawa ◽  
H. Yamane ◽  
M. Takayama ◽  
K. Sunami ◽  
Y. Nakai

2017 ◽  
Author(s):  
Nikola Ciganović ◽  
Rebecca L. Warren ◽  
Batu Keçeli ◽  
Stefan Jacob ◽  
Anders Fridberger ◽  
...  

AbstractThe cochlea not only transduces sound-induced vibration into neural spikes, it also amplifies weak sound to boost its detection. Actuators of this active process are sensory outer hair cells in the organ of Corti, whereas the inner hair cells transduce the resulting motion into electric signals that propagate via the auditory nerve to the brain. However, how the outer hair cells modulate the stimulus to the inner hair cells remains unclear. Here, we combine theoretical modeling and experimental measurements near the cochlear apex to study the way in which length changes of the outer hair cells deform the organ of Corti. We develop a geometry-based kinematic model of the apical organ of Corti that reproduces salient, yet counter-intuitive features of the organ’s motion. Our analysis further uncovers a mechanism by which a static length change of the outer hair cells can sensitively tune the signal transmitted to the sensory inner hair cells. When the outer hair cells are in an elongated state, stimulation of inner hair cells is largely inhibited, whereas outer hair cell contraction leads to a substantial enhancement of sound-evoked motion near the hair bundles. This novel mechanism for regulating the sensitivity of the hearing organ applies to the low frequencies that are most important for the perception of speech and music. We suggest that the proposed mechanism might underlie frequency discrimination at low auditory frequencies, as well as our ability to selectively attend auditory signals in noisy surroundings.Author summaryOuter hair cells are highly specialized force producers inside the inner ear: they can change length when stimulated electrically. However, how exactly this electromotile effect contributes to the astonishing sensitivity and frequency selectivity of the inner ear has remained unclear. Here we show for the first time that static length changes of outer hair cells can sensitively regulate how much of a sound signal is passed on to the inner hair cells that forward the signal to the brain. Our analysis holds for the apical region of the inner ear that is responsible for detecting the low frequencies that matter most in speech and music. This shows a mechanisms for how frequency-selectivity can be achieved at low frequencies. It also opens a path for the efferent neural system to regulate hearing sensitivity.


1990 ◽  
Vol 109 (1-2) ◽  
pp. 49-56 ◽  
Author(s):  
S. D. Comis ◽  
M. P. Osborne ◽  
D. J. R. Jeffries

2021 ◽  
Author(s):  
Sanjeewa Abeytunge ◽  
Francesco Gianoli ◽  
A.J. Hudspeth ◽  
Andrei S. Kozlov

AbstractHair cells, the receptors of the inner ear, detect sounds by transducing mechanical vibrations into electrical signals. From the top surface of each hair cell protrudes a mechanical antenna, the hair bundle, which the cell uses to detect and amplify auditory stimuli, thus sharpening frequency selectivity and providing a broad dynamic range. Current methods for mechanically stimulating hair bundles are too slow to encompass the frequency range of mammalian hearing and are plagued by inconsistencies. To overcome these challenges, we have developed a method to move individual hair bundles with photonic force. This technique uses an optical fiber whose tip is tapered to a diameter of a few micrometers and endowed with a ball lens to minimize divergence of the light beam. Here we describe the fabrication, characterization, and application of this optical system and demonstrate the rapid application of photonic force to vestibular and cochlear hair cells.


1987 ◽  
Vol 96 (1_suppl) ◽  
pp. 48-50 ◽  
Author(s):  
P. A. Leake ◽  
R. L. Snyder ◽  
C. E. Schreiner

The coadministration of kanamycin (400 mg/kg body weight, s.c.) and aminooxyacetic acid (25 mg/kg body weight, s.c.) results in rapid, total destruction of cochlear hair cells in cats. This drug combination is safer and the time course of hearing losses is less variable than with administration of aminoglycosides alone. Uniform survival of spiral ganglion neurons at 2 and 4 weeks after drug administration suggests a time course similar to that previously observed in neomycin-deafened cats, but more data with longer survival periods are needed to verify these preliminary observations.


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