A general model of inner ear pressure responses including ultra‐low frequencies

1999 ◽  
Vol 105 (2) ◽  
pp. 1085-1085
Author(s):  
Ernst‐J. Haberland ◽  
Hans J. Neumann
1989 ◽  
Vol 257 (3) ◽  
pp. F341-F346 ◽  
Author(s):  
E. Bartoli ◽  
A. Satta ◽  
F. Melis ◽  
M. A. Caria ◽  
W. Masala ◽  
...  

We tested the hypothesis that changes in extracellular fluid volume are reflected by pressure changes within structures of the inner ear and that through neural pathways, a control mechanism exerts an influence on antidiuretic hormone (ADH) release and Na excretion. The study was performed on 35 guinea pigs. In protocol 1, 13 animals were studied before and after decompression of the inner ear by bilateral fluid withdrawal in an experimental setting of sustained isotonic expansion that kept the osmoreceptor partially activated and the intrathoracic volume receptors suppressed. A group of six sham-operated animals served as control. In protocol 2, nine animals were studied before and after a unilateral rise in their inner ear pressure during slightly hypertonic low-rate infusions that kept the osmoreceptor and thoracic volume receptors stimulated. A group of seven sham-operated guinea pigs served as controls. Decompression of the inner ear was attended by a rise in plasma ADH from 11.9 +/- 2.4 to 29.1 +/- 6.9 pg/ml, in urine osmolality (Uosmol) from 470 +/- 48 to 712 +/- 46 mosmol/kg (P less than 0.001), and a fall in urine flow rate (V) from 184 +/- 47 to 71 +/- 11 microliters/min (P less than 0.01), whereas plasma Na (PNa) and osmolality (Posmol) did not change. During inner ear hypertension, plasma ADH fell from 25.6 +/- 3.9 to 18.4 +/- 3.1, Uosmol from 829 +/- 58 to 627 +/- 43 (P less than 0.001), and V rose from 51 +/- 11 to 130 +/- 23 (P less than 0.001), whereas glomerular filtration rate, PNa, and Posmol did not change.(ABSTRACT TRUNCATED AT 250 WORDS)


2001 ◽  
Vol 22 (4) ◽  
pp. 534-538 ◽  
Author(s):  
Cuneyt Yilmazer ◽  
Levent Sennaroglu ◽  
Figen Basaran ◽  
Gonca Sennaroglu

2014 ◽  
Vol 1 (2) ◽  
pp. 140166 ◽  
Author(s):  
Kathrin Kugler ◽  
Lutz Wiegrebe ◽  
Benedikt Grothe ◽  
Manfred Kössl ◽  
Robert Gürkov ◽  
...  

Noise-induced hearing loss is one of the most common auditory pathologies, resulting from overstimulation of the human cochlea, an exquisitely sensitive micromechanical device. At very low frequencies (less than 250 Hz), however, the sensitivity of human hearing, and therefore the perceived loudness is poor. The perceived loudness is mediated by the inner hair cells of the cochlea which are driven very inadequately at low frequencies. To assess the impact of low-frequency (LF) sound, we exploited a by-product of the active amplification of sound outer hair cells (OHCs) perform, so-called spontaneous otoacoustic emissions. These are faint sounds produced by the inner ear that can be used to detect changes of cochlear physiology. We show that a short exposure to perceptually unobtrusive, LF sounds significantly affects OHCs: a 90 s, 80 dB(A) LF sound induced slow, concordant and positively correlated frequency and level oscillations of spontaneous otoacoustic emissions that lasted for about 2 min after LF sound offset. LF sounds, contrary to their unobtrusive perception, strongly stimulate the human cochlea and affect amplification processes in the most sensitive and important frequency range of human hearing.


1998 ◽  
Vol 118 (5) ◽  
pp. 703-708 ◽  
Author(s):  
Eugene N. Myers ◽  
Shingo Murakami ◽  
Kiyofumi Gyo ◽  
Richard L. Goode

Velocity of malleus, umbo, and stapes footplate in response to stepwise increases up to +400 mm H2O in hydrostatic pressure of the inner ear was investigated in 10 fresh human temporal bones by using a laser Doppler interferometer. The sound-pressure input was 114 dB SPL, and the frequency range was 0.4 to 5.0 kHz. Static displacement of these sites was also measured by a video measuring system. When the inner ear pressure was increased, the malleus and stapes moved outward. Amplitude of umbo velocity decreased below 1.0 kHz with a slight increase around 2.0 kHz, whereas stapes velocity decreased at all frequencies with the major effect below 1.0 kHz. The phase angle of malleus umbo velocity advanced markedly in response to the increased inner ear pressure between 1.0 and 1.4 kHz. Change in the vibration of the umbo was thought to be primarily caused by an increased stiffness of the middle ear conduction system, and that of the stapes was caused by distention of the annular ligament and increased cochlear impedance produced by the increased inner ear pressure. These changes in TM vibration and its phase angle may help detect indirectly an elevation of inner ear pressure. (Otolaryngol Head Neck Surg 1998;118:703–8.)


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.


2001 ◽  
Vol 121 (4) ◽  
pp. 470-476 ◽  
Author(s):  
E.O. Thalen ◽  
H.P. Wit ◽  
J.M. Segenhout ◽  
F.W.J. Albers

Sign in / Sign up

Export Citation Format

Share Document