Outer Hair Cell Somatic Electromotility In Vivo and Power Transfer to the Organ of Corti

AbstractThe active amplification of sound-induced vibrations in the cochlea, known to be crucial for auditory sensitivity and frequency selectivity, is not well understood. The outer hair cell (OHC) somatic electromotility is a potential mechanism for such amplification. Its effectiveness in vivo is putatively limited by the electrical low-pass filtering of the cell's transmembrane potential. However, the transmembrane potential is an incomplete metric. We propose and estimate two metrics to evaluate the effectiveness of OHC electromotility in vivo. One metric is the OHC electromechanical ratio defined as the amplitude of the ratio of OHC displacement to the change in its transmembrane potential. The in vivo electromechanical ratio is derived from the recently measured in vivo displacements of the reticular lamina and the basilar membrane at the 19 kHz characteristic place in guinea pigs and using a model. The ratio, after accounting for the differences in OHC vibration in situ due to the impedances from the adjacent structures, is in agreement with the literature values of the in vitro electromechanical ratio measured by others. The second and more insightful metric is the OHC somatic power. Our analysis demonstrates that the organ of Corti is nearly optimized to receive maximum somatic power in vivo and that the estimated somatic power could account for the active amplification

Dynamic aspects of guinea pig inner hair cell receptor potentials with transient asphyxia

DC and AC receptor potentials of cochlear inner hair cells in response to tone bursts of various frequencies and intensities were continuously measured during and following periods of transient asphyxia. The effects of asphyxia were most pronounced for low sound pressure level (SPL) acoustic stimuli near the characteristic frequency (CF) of the inner hair cell, leading to vulnerability of the `tip' of the cell's frequency tuning curve (FTC). The resulting changes in the shape of the FTC are, first, a reduction in tip criterion sensitivity of 10-20 dB without significant loss in sharpness of tuning. Later, when the full effect of 30-45 s asphyxia occurs, tip sensitivity loss between 30 and 65 dB is accompanied by greatly broadened tuning and a shift downward in frequency of the CF by greater than 1/4 octave. The CF shift is due to a progressive loss of high frequency sensitivity. The linear segment of the input-output (intensity) function, plotted as log DC receptor potential versus SPL (at the original CF), becomes longer during the early phase asphyxia, and the slope of the segment declines by 50%. At high SPLs, for all frequencies, the time course of the receptor potential change was similar in shape to that exhibited by the endocochlear potential (EP). In particular, for high sound levels, the recovery of response matches the EP while for low level tip frequency sounds recovery is protracted. No difference between the decline of the AC and DC receptor potentials at CF was observed. Inner hair cell resting membrane potential (Em) hyperpolarized during asphyxia by 2-6 mV, correlating with the change in EP according to a ratio of 1/10 (Em/EP).Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/24670/1/0000083.pd

Velocity of red blood cell flow in capillaries of the guinea pig cochlea

Velocities of red blood cells (RBCs) in the lateral wall of the cochlea were determined in the anesthetized guinea pig from direct optical microscopic observations. Mean flow velocity of the blood was measured by timing the passage of a fluorescently-labeled subpopulation of RBCs across a measured capillary length. The optical observations were achieved using an intravital microscope equipped for epifluorescence and the measurements were derived from video images acquired with an image intensified television camera. In the third turn of the cochlea the velocity of RBCs differed significantly between two major classes of capillaries. The mean velocity in spiral ligament vessels was 0.12 mm/s while stria vascularis flow was slower (0.08 mm/s). In a typical animal, the range of velocities among different vessels of the ligament was 0.09-0.18 mm/s while it was 0.03-0.10 mm/s for stria vascularis vessels. Corresponding to this velocity difference, the apparent mean vessel diameters for the two types of vessels also differed. Spiral ligament capillaries were 9.3 [mu]m while striai capillaries were 12.2 [mu]m in diameter. Comparison of flow velocity in different turns of the cochlea indicated that the distribution of blood velocity throughout the cochlea lateral wall is constant.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/26888/1/0000454.pd

An Overview of Electrically Evoked Otoacoustic Emissions in the Mammalian Cochlea

AbstractAlternating currents injected into the cochlea are able to evoke outer hair cell-mediated basilar membrane motion, thus give rise to production of otoacoustic emissions. This electrically evoked otoacoustic emission(EEOAE) provides a useful tool for the research of out hair cell electromotility in vivo. This article reviews the research work on EEOAEs in mammals. Features of the EEOAEs and theories of their generation are introduced. Methods of EEOAE measurement are also described

The influence of NF-ΚB signal-transduction pathways on the murine inner ear by acoustic overstimulation

Nuclear factor-kappa B (NF-ΚB) comprises a family of inducible transcription factors that serve as important regulators of the host immune and inflammatory responses. The NF-ΚB signals are activated via the canonical and/or noncanonical pathways in response to diverse stimuli. The excessive action of NF-ΚB signal-transduction pathways frequently causes self-injurious phenomena such as allergic diseases, vascular disorders, and ischemia–reperfusion neuronal damage. In the inner ear, the role of NF-ΚB has not been clarified because the activated NF-ΚB signals potentially induce both cytoprotective and cytotoxic target genes after ototoxic stimulation. In the present study, we investigated the response of NF-ΚB in both the canonical and noncanonical pathways to acoustic overstimulation (117 dB/SPL/2 hr) and followed the change of inflammatory factors (inducible nitric oxide synthase [iNOS], intracellular adhesion molecule-1 [ICAM-1], and vascular cell adhesion molecule-1 [VCAM-1]) in the cochlear lateral wall (CLW) and the rest of cochlea (RoC). By means of immunohistochemistry combined with confocal microscopy and reverse transcriptase–polymerase chain reaction techniques, we found the response of NF-ΚB family members (NF-ΚB1, 2, RelA, and RelB) at the transcription level. After the NF-ΚB signaling, the inflammatory factors were significantly increased in the CLW and the RoC. Additionally, at the protein level, the prominent expression of adhesion molecules (ICAM-1 and VCAM-1) was observed in the tissue around the capillaries in the stria vascularis. These results show that acoustic overstimulation causes the NF-ΚB signaling to overexpress the inflammatory factors in the inner ear, and the up-regulation of the adhesion molecules (ICAM-1 and VCAM-1) and iNOS potentially influence the hemodynamics and the cellular integrity in the stria vascularis. © 2009 Wiley-Liss, Inc.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/62147/1/22018_ftp.pd

Spontaneous Basilar-Membrane Oscillation (SBMO) and Coherent Reflection

In a previous report (in JARO) we have described a relatively high-frequency (15 kHz) spontaneous oscillation of the basilar membrane (SBMO) in a guinea pig ear; this oscillation was accompanied by a spontaneous otoacoustic emission (SOAE) at the same frequency. During the spontaneous oscillation and after it had subsided, the mechanical frequency response of the basilar membrane was measured by way of a wide-band random-noise stimulus, and it showed a number of spectral peaks, one of which having the frequency of the original oscillation. This pattern of peaks cannot be explained by assuming a single place of reflection in the cochlea. In this paper the process of ‘coherent reflection’ is artificially evoked in a three-dimensional model of the cochlea by imposing random place-fixed irregularities to the basilar-membrane impedance. It is shown that in the model a series of peaks arises in the frequency spectrum of the basilar-membrane response which phenomenon resembles the one found in the experimental animal. It is also shown that these peaks are actually due to superposition of the primary wave and a wave resulting from ‘coherent reflection’ which is reflected at the stapes. When the intensity of the acoustic stimulus signal is increased, the relative sizes of these peaks in the simulation diminish in about the same way as in the experiment. It is concluded that coherent reflection most likely is the cause of the ‘extra peaks’, and that this concept can also explain the observed level dependence of these peaks. The findings of this study lead to a minor refinement regarding the actual requirements for coherent reflection to arise.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/41389/1/10162_2005_Article_20.pd

Laser doppler measurements of cochlear blood flow during loud sound exposure in the guinea pig

This investigation examined the effects of loud sound of different frequencies and intensities on cochlear blood flow as measured by the laser Doppler flowmeter. Cochlear blood flow was measured in anesthetized guinea pigs during a l h exposure to either a 2, 4, or 12 kHz pure tone or high-pass noise (10-40 kHz) at 90, 103, or 110 dB SPL. Cochlear function was assessed using the compound action potential audiogram before and after exposure. There was no change in blood flow in the second turn with a 2, 4, or 12 kHz tone but there was a significant (P < 0.05) decline in flow in the first cochlear turn at the end of either the 12 kHz tone or high-pass noise exposure at 103 and 110 dB SPL. There were elevations in the thresholds of the cochlear compound action potential after all but the 90 dB exposures to 12 kHz or high-pass noise. No such changes were observed in blood flow or electrophysiology in control animals. These findings demonstrate that there is a small but significant decline in cochlear blood flow with high intensity sound exposure. However, the relationship between this change in blood flow and the development of cochlear damage is unclear.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/26841/1/0000401.pd

Cochlear microphonic enhancement in two tone interactions

Two tone interaction functions of the cochlear microphonic (CM) were obtained from pigmented guinea pigs. First (basal) cochlear turn recording locations show optimally enhanced levels of CM when the interfering tone (F2) was positioned about 4 kHz above probe tones (F1) of 12 kHz and 20 kHz. Maximum enhancement occurred for equal level tones. No enhancement was seen for a probe tone of 4 kHz. When basal turn cochlear sensitivity was compromised, CM enhancement caused by the interfering tone was altered and only CM reduction was then seen. The CM reduction was the typical characteristic described by many earlier studies. Guinea pigs with various changes in cochlear sensitivity were studied, providing evidence in support of earlier reports that CM interference (both reductions and enhancements) depends on far field vector summation of the outputs of hair cells from a restricted area of the basilar membrane. No CM enhancement was seen in micropipette recordings from within the organ of Corti.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/29482/1/0000568.pd

In vivo capillary diameters in the stria vascularis and spiral ligament of the guinea pig cochlea

Blood microvessels in the membranous lateral wall of the cochlea were examined using intravital microscopic techniques. A video analysis system made serial diameter measurements at 1 [mu]m intervals along the length of selected vessel segments during four experimental conditions. For each vessel segment, the serial measurements were statistically converted into a single diameter estimate, such that the flow resistance in a uniform vessel of this diameter would equal the resistance of the real non-uniform vessel.Nominal vessel diameters found (spiral ligament: 9-12 [mu]m; stria vascularis: 12-16 [mu]m) were nearly double those reported earlier in histological observations (Axelsson, 1968). During stimulation the largest diameter change seen was a 3.7% dilation (about 0.5 [mu]m) in response to breathing 5% CO2 in oxygen. Theoretically, this change could reduce vascular fluid resistance by 16%, nearly enough to explain the observed flow increase of 20%. No diameter changes occurred for 5% CO2 in air despite a 50% flow increase, nor for air pressure pulses applied at the tympanic membrane. Round window electrical stimulation of 50 [mu]A also produced dilation (< 2.5%), but higher current levels were ineffective. In general, blood flow increases seen in this study could not adequately be attributed to the small lateral wall vessel diameter increases nor systemic causes, suggesting that lateral wall blood flow in these instances is dependent on control within the modiolus.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/27311/1/0000332.pd