Cochlear Micromechanics and Macromechanics

Patuzzi, Robert

doi:10.1007/978-1-4612-0757-3_4

Cited by 142 publications

(122 citation statements)

References 132 publications

Supporting

Mentioning

117

Contrasting

Unclassified

Order By: Relevance

“…Overall, findings are consistent with the idea that the basilar membrane response to a particular frequency depends on the action of active elements basal to the characteristic frequency (CF) place (Geisler et al 1990;Patuzzi 1996). Other physiological measures have also implicated distribution of the active elements responsible for frequency-specific amplification being basal to the CF place.…”

Section: Basal Contributions To Sl Teoae Componentssupporting

confidence: 84%

Basal Contributions to Short-Latency Transient-Evoked Otoacoustic Emission Components

Lewis

Goodman

2014

JARO

View full text Add to dashboard Cite

The presence of short-latency (SL), less compressivegrowing components in bandpass-filtered transientevoked otoacoustic emission (TEOAE) waveforms may implicate contributions from cochlear regions basal to the tonotopic place. Recent empirical work suggests a region of SL generation between ∼1/5 and 1/10-octave basal to the TEOAE frequency's tonotopic place. However, this estimate may be biased to regions closer to the tonotopic place as the TEOAE extraction technique precluded measurement of components with latencies shorter than ∼5 ms. Using a variant of the non-linear, double-evoked extraction paradigm that permitted extraction of components with latencies as early as 1 ms, the current study empirically estimated the spatial-extent of the cochlear region contributing to 2 kHz SL TEOAE components. TEOAEs were evoked during simultaneous presentation of a suppressor stimulus, in order to suppress contributions to the TEOAE from different places along the cochlear partition. Three or four different-latency components of similar frequency content (∼2 kHz) were identified for most subjects. Component latencies ranged from 1.4 to 9.6 ms; latency was predictive of the component's growth rate and the suppressor frequency to which the component's magnitude was most sensitive to change. As component latency decreased, growth became less compressive and suppressor-frequency sensitivity shifted to higher frequencies. The shortest-latency components were most sensitive to suppressors approximately 3/5-octave higher than their nominal frequency of 2 kHz. These results are consistent with a distributed region of generation extending to approximately 3/5-octave basal to the TEOAE frequency's tonotopic place. The empirical estimates of TEOAE generation are similar to model-based estimates where generation of the different-latency components occurs through linear reflection from impedance discontinuities distributed across the cochlear partition.

show abstract

Section: Basal Contributions To Sl Teoae Componentssupporting

confidence: 84%

Basal Contributions to Short-Latency Transient-Evoked Otoacoustic Emission Components

Lewis

Goodman

2014

JARO

View full text Add to dashboard Cite

show abstract

“…Many models of cochlear mechanics assume that the vibration pattern in the cochlea is well described by propagating fluid waves (Patuzzi, 1996). The ratio of wavelength and depth of the fluid in the scalae is an important parameter in such models.…”

Section: Panoramic Phase Analysis In the Apexmentioning

confidence: 99%

Panoramic Measurements of the Apex of the Cochlea

Heijden¹,

Joris²

2006

J. Neurosci.

View full text Add to dashboard Cite

Our understanding of cochlear mechanics is impeded by the lack of truly panoramic data. Sensitive mechanical measurements cover only a narrow cochlear region, mostly in the base. The global spatiotemporal pattern of vibrations along the cochlea cannot be inferred from such local measurements but is often extrapolated beyond the measurement spot under the assumption of scaling invariance. Auditory nerve responses give an alternative window on the entire cochlea, but traditional techniques do not allow recovery of the effective vibration pattern. We developed a new analysis technique to measure cochlear amplitude and phase transfer of fibers with characteristic frequencies Ͻ5 kHz. Data from six cats yielded panoramic phase profiles along the apex of the cochlea for an ϳ5 octave range of stimulus frequencies. All profiles accumulated systematic phase lags from base to apex. Phase accumulation was not gradual but showed a two-segment character: a steep segment (slow propagation) around the characteristic position of the stimulus, and a shallow segment (fast propagation) basal to it. The transition between the segments occurred in a narrow region and was smooth. Wavelength near characteristic position decreased from ϳ3.5 to ϳ1 mm for frequencies from 200 to 4000 Hz, corresponding to phase velocities of ϳ0.5 to ϳ5 m/s. The accumulated phase lag between the eardrum and characteristic position varied from ϳ1 cycle at 200 Hz to ϳ2.5 cycle at 4 kHz, invalidating scaling invariance. The generic character of our analysis technique and its success in solving the difficult problem of reconstructing the effective sensory input from neural recordings suggest its wider application as a powerful alternative to customary system analysis techniques.

show abstract

“…4B, Table 3B). DPOAEs are sound emissions from the ear, which are produced by pairs of tones that interact nonlinearly to produce extra tones (Patuzzi 1996). These tones are now thought to be produced by an overlap of the actively amplified traveling waves on the basilar membrane (Probst et al 1991;Zureck 1985).…”

Section: Novel Th-dependent Processes During the Critical Developmentmentioning

confidence: 99%

“…The active mechanisms in the cochlea are driven by hair cell electromotility, which is in turn dependent on a functional mechanoelectrical transduction of acoustic stimuli, as well as on intact endocochlear and membrane potentials (for a review, see Dallos and Evans 1995). The observed impairment of DPOAEs may thus be due either to impaired mechanoelectrical or electromechanical transduction or impaired endocochlear potential (EP), one of the driving forces for electromotility (for a review see, Patuzzi 1996). Although thyroid hormone receptors have been found to be expressed in OHCs (Knipper et al 1998;Lautermann and Ten Cate 1997), so far neither of the processes that are the driving forces for electromotility have been shown to be controlled by TH.…”

Section: Novel Th-dependent Processes During the Critical Developmentmentioning

confidence: 99%

Thyroid Hormone Deficiency Before the Onset of Hearing Causes Irreversible Damage to Peripheral and Central Auditory Systems

Knipper

Zinn

Maier

et al. 2000

Journal of Neurophysiology

169

156

View full text Add to dashboard Cite

Thyroid hormone deficiency before the onset of hearing causes irreversible damage to peripheral and central auditory systems. J. Neurophysiol. 83: 3101-3112, 2000. Both a genetic or acquired neonatal thyroid hormone (TH) deficiency may result in a profound mental disability that is often accompanied by deafness. The existence of various TH-sensitive periods during inner ear development and general success of delayed, corrective TH treatment was investigated by treating pregnant and lactating rats with the goitrogen methimazole (MMI). We observed that for the establishment of normal hearing ability, maternal TH, before fetal thyroid gland function on estrus days 17-18, is obviously not required. Within a crucial time between the onset of fetal thyroid gland function and the onset of hearing at postnatal day 12 (P12), any postponement in the rise of TH-plasma levels, as can be brought about by treating lactating mothers with MMI, leads to permanent hearing defects of the adult offspring. The severity of hearing defects that were measured in 3-to 9-mo-old offspring could be increased with each additional day of TH deficiency during this critical period. Unexpectedly, the active cochlear process, assayed by distortion product otoacoustic emissions (DPOAE) measurements, and speed of auditory brain stem responses, which both until now were not thought to be controlled by TH, proved to be TH-dependent processes that were damaged by a delay of TH supply within this critical time. In contrast, no significant differences in the gross morphology and innervation of the organ of Corti or myelin gene expression in the auditory system, detected as myelin basic protein (MBP) and proteolipid protein (PLP) mRNA using Northern blot approach, were observed when TH supply was delayed for few days. These classical TH-dependent processes, however, were damaged when TH supply was delayed for several weeks. These surprising results may suggest the existence of different TH-dependent processes in the auditory system: those that respond to corrective TH supply (e.g., innervation and morphogenesis of the organ of Corti) and those that do not, but require T3 activity during a very tight time window (e.g., active cochlear process, central processes).

show abstract

Cochlear Micromechanics and Macromechanics

Cited by 142 publications

References 132 publications

Basal Contributions to Short-Latency Transient-Evoked Otoacoustic Emission Components

Basal Contributions to Short-Latency Transient-Evoked Otoacoustic Emission Components

Panoramic Measurements of the Apex of the Cochlea

Thyroid Hormone Deficiency Before the Onset of Hearing Causes Irreversible Damage to Peripheral and Central Auditory Systems

Contact Info

Product

Resources

About