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At least 523 records · Page 29Linked to original sources
PubMed2005

Mechanisms of noise-induced hearing loss potentiation by hypoxia.

Potentiation of noise-induced permanent threshold shift (PTS) by hypoxia has been reported [Hear. Res. 172 (1-2) (2002) 186]. In this study in rats, effects of noise (110 dB SPL), hypoxia (10% O(2)), and their combination have been determined on different cochlear potentials and on the expression of genes coding proteins in the outer hair cell (OHC) membrane skeleton (beta-actin) and in the mitochondrial respiratory chain (SDHa & b). The noise exposure alone caused CAP threshold shift only in the noise-band. The combined exposure to noise and hypoxia caused an about 40-dB PTS at all frequencies within and above the noise band. Loss of the cochlear amplification was not always related to the CM-suppression. SP was only affected at high frequencies by the combined exposure. Gene expression of beta-actin was up-regulated by the noise exposure, which was blocked by hypoxia. Gene expression of SDHa was also up-regulated by the noise and the combined exposure. The data suggest that loss of the cochlear active process, due to damage to the OHC membrane skeleton and to the cellular energy generation system, is related to the noise-induced hearing loss potentiation by hypoxia. Inner hair cell damage may also be involved in the hypoxia potentiation in the basal turn.

Actins↗
PubMed1982

Recovery from prolonged sensorineural hearing loss.

Five cases of sensorineural hearing loss are presented in which partial or complete recovery of hearing occurred after periods of deafness lasting from three months to more than five years. Three of the cases were diagnosed as Meniere's disease, one as sudden deafness of probable viral origin, and one as idiopathic sudden deafness. A review of the literature reveals brief mention of only a few similar cases, although it is suspected that the phenomenon is not as rare as these isolated reports suggest. It is proposed on the basis of experimental work in animals that the reversible deafness in these patients may be due to temporary obstruction of capillaries in the stria vascularis, which produces strial hypoxia resulting in a reduction in the endolymphatic potential, with consequent hearing loss.

Adult↗
PubMed1997

Microphonic and DPOAE measurements suggest a micromechanical mechanism for the 'bounce' phenomenon following low-frequency tones.

Neural auditory thresholds in the guinea pig can be temporarily improved by up to 6 dB about 2 min after the cessation of an moderately intense low-frequency tone (Kirk and Patuzzi, 1997). We have measured changes in the f2-f1 distortion product otoacoustic emission (DPOAE) and low-frequency microphonic potential in scala tympani before, during and after a low-frequency tone (200 Hz) to determine the cause of this so-called bounce phenomenon. In particular we have analysed the low-frequency microphonic waveform in detail to estimate changes in the maximal receptor current through the outer hair cells (OHCs), the sensitivity of the OHC forward transduction process and the change in OHC operating point on the mechano-electrical transduction transfer curve. Our results indicate that a 200 Hz tone changes the maximal current and sensitivity of the OHCs minimally, but more importantly, it transiently changes the operating point on the OHC transfer curve. In particular, the operating point changes are consistent with a movement of the OHC stereocilia away from the OHC basal body at the peak of the bounce. These changes detected using the microphonic potential are associated with changes in the level of the f2-f1 DPOAE that correlate well with the electrical measurements. We suggest that the shift in operating point is largely responsible for the increase in cochlear sensitivity, and is due to a disruption of the salt balance within the cochlea during the intense low-frequency tone.

Acoustic Stimulation↗
PubMed1996

Correlative evidence of hypertension and altered cochlear microhomeostasis: electrophysiological changes in the spontaneously hypertensive rat.

The spontaneously hypertensive rat model has been used to show that hypertension is an important pathophysiological risk factor in age-related hearing loss. In the present study, compound action potential (CAP), electrochemical potential (ECP), and potassium concentration (CK+) measurements were taken from the cochlea of genetically predisposed, spontaneously hypertensive rats (SHR) and from normotensive Wistar-Kyoto (WKY) rats. In the SHR model, as the duration of hypertension increased with the animal's age (from 3 to 8 months), CAP thresholds increased, ECP increased in marginal cells only, and CK+ increased in both endolymph and marginal cells. Collectively, the data suggest that ionic alternations of cellular potentials are involved in hearing changes in the hypertensive state. Ultimately, such data may assist in understanding hearing loss in individuals who are diagnosed with hypertension.

Action Potentials↗
PubMed1986

Electrically evoked potentials in cochlear implant subjects.

A series of experiments was performed to study electrically evoked potentials as indicators of subject response to cochlear implantation. 1. Brain stem evoked responses to electrical stimulation were compared to those obtained by acoustic stimulation in guinea pigs. The response pattern was similar and was independent of the site of placement of the stimulus electrode (cochlear base or apex) or of the extracochlear ground electrode (eustachian tube or temporalis muscle) when evoked electrically. 2. Electrically evoked middle latency responses were recorded and compared to subjective behavioral thresholds in patients who had received a single channel cochlear implant (House-Urban). The behavioral responses to the same stimuli were similar. 3. Electrically evoked auditory brain stem responses were studied in single channel cochlear implant subjects (3M/House). When evoked electrically, potential latencies were shorter and interpeak intervals narrower than acoustically evoked potentials.

Acoustic Stimulation↗
PubMed1994

Intraoperative monitoring of auditory function: experimental observations and new applications.

The three different methods of intraoperative monitoring, namely, auditory brainstem response evaluation (ABR), electrocochleography (ECoG), and direct eighth nerve compound action potentials monitoring are reviewed. Both ECoG and direct eighth nerve monitoring surpass the ABR in their ability to provide fast, almost instantaneous, large, reproducible potentials in response to click stimuli. Changes in the amplitude and the latency of these potentials alert the surgeon of an impending eighth nerve injury. Human clinical observations revealed instances of persistence of the ECoG despite a total eighth nerve section in the cerebellopontine angle. Animal and human experiments were conducted to evaluate the effectiveness of ECoG and direct eighth nerve monitoring in hearing preservation. Twelve cats underwent progressive sectioning of the eighth nerve with simultaneous monitoring of changes in their ECoG and direct eighth nerve potentials. ECoG thresholds were obtained intraoperatively in eight patients undergoing surgery for conductive hearing loss. The results of these experiments suggest that recording directly from the eighth nerve is a more accurate technique during cerebellopontine angle and eighth nerve surgery. ECoG, however, appears to have a promising role in the intraoperative monitoring of middle ear reconstruction procedures under general anesthesia.

Action Potentials↗
PubMed1998

CD1 hearing-impaired mice. II. Group latencies and optimal f2/f1 ratios of distortion product otoacoustic emissions, and scanning electron microscopy.

In our companion paper (Le Calvez et al., 1998), the levels of distortion product otoacoustic emissions (DPOAE) were collected in the ears of CD1 mice with progressive degeneration of cochlear outer hair cells (OHC). Their comparison to standard functional measurements such as auditory-evoked brainstem responses (ABR) showed that CD1 ears could be classified as normal or impaired in a frequency-specific manner using DPOAE levels. The present work reports how DPOAE phases and levels of young CD1 mice were affected by varying the frequency ratio of eliciting stimuli at frequencies f1 and f2. Normally hearing CBA/J mice served as controls. The rate of phase change of DPOAE when f1 was varied and f2 was fixed allowed the group delay of DPOAE to be derived. The changes of DPOAE levels during this procedure disclosed bandpass characteristics that several reports (Fahey and Allen, 1986; Brown and Gaskill, 1990) assumed to be the reflection of important features of cochlear micromechanics, possibly in relation to the coupling of OHCs to the tectorial membrane. Group delays became significantly shorter when ABR thresholds exceeded 40 dB elevation. The bandpass filter characteristics strikingly depended on auditory function so that the optimal ratio f2/f1 progressively shifted from 1.24 to 1.50 or more when hearing loss increased. A difference was also noted between CD1 ears whose ABR thresholds were not yet increased and control CBA/J (optimal ratio 1.20). Scanning electron microscopy disclosed a variety of often minor OHC lesions that were only roughly correlated with cochlear function. However, the presence of abnormalities in the reticular lamina associated with early changes of DPOAE fine structure as a function of f2/f1 supported the hypothesis of some involvement of micromechanical features in the bandpass filter characteristics of DPOAE. The sensitivity of their measurement in pathological situations is potentially interesting.

Animals↗
PubMed2003

Mechanical leverage in the middle ear of the American bullfrog, Rana catesbeiana.

Textbooks lump the middle ears of 'submammalian Tetrapoda' as being 'one-ossicle ears'. Conventionally the anuran middle ear is depicted with a shaft-like skeletal unit connecting the tympanic membrane to the inner ear. This shaft comprises mediad a long bony columella and laterad a short cartilaginous extracolumella. But dissection of Rana catesbeiana ears showed: the extracolumella, as long as the columella, is proximally expanded in the vertical plane, forming dorsal and ventral heads. The medio-dorsal head is movably jointed to the columella, between these two there is an obtuse angle ventrad; the extracolumellar medio-ventral head is anchored by a ligament to the middle-ear cavity ceiling. When the tympanic membrane moves outwards, pulling the extracolumella, the medio-dorsal head of the extracolumella must be forced inwards, rotating on the ventral anchorage, pushing the columella towards the inner ear. The ossicular chain thus includes a mechanical lever, possessing the magnitude of the ratio length:width of the extracolumella; this is additional to the lever known from the columellar footplate, which rotates on its firm ventral attachment. These levers are confirmed physiologically, by the difference between the inner-ear sensitivity (shown by isopotential audiograms of microphonic potentials) when stimulated by a vibrator first at the tympanic membrane, then at the proximal stump of the amputated columella. Perusal of the primary literature showed that this morphology is widespread among anuran ears.

Acoustic Stimulation↗
PubMed1999

Signs of endolymphatic hydrops after perilymphatic perfusion of the guinea pig cochlea with cholera toxin; a pharmacological model of acute endolymphatic hydrops.

There are indications that endolymph homeostasis is controlled by intracellular cAMP levels in cells surrounding the scala media. Cholera toxin is a potent stimulator of adenylate cyclase, i.e. it increases cAMP levels. We hypothesized that perilymphatic perfusion of cholera toxin might increase endolymph volume by stimulating adenylate cyclase activity, providing us with a pharmacological model of acute endolymphatic hydrops (EH). Guinea pig cochleas were perfused with artificial perilymph (15 min), with or without cholera toxin (10 microg/ml). The endocochlear potential (EP) was measured during and after perfusion. The summating potential (SP), evoked by 2, 4 and 8 kHz tone bursts, was measured via an apically placed electrode 0, 1, 2, 3 and 4 h after perfusion. Thereafter, the cochleas were fixed to enable measurement of the length of Reissner's membrane, reflecting EH. After perfusion the EP increased significantly over time in the cholera toxin group as compared to the controls. Also, the SP increased gradually at all frequencies in the cholera toxin group. Comparison within animals showed that the increase in SP became significant after 2 h at 4 kHz, after 3 h at 2 kHz and after 4 h at 8 kHz. In the control group the SP did not change significantly. The compound action potential (CAP) amplitude decreased monotonically over time at all frequencies in both the cholera toxin group and the control group, but it decreased faster in the cholera toxin group. Also, the cochlear microphonics amplitude decreased over time at all frequencies in both groups, but the decrease was significant only in the cholera toxin group after 3 h at 2 and 4 kHz. Quantification of the length of Reissner's membrane showed a small but insignificant enlargement in the cholera toxin treated animals compared to controls. These results are in accord with our view that EH is accompanied by an increase in SP and a decrease in CAP. Our results partially confirm previous results of Feldman and Brusilow (Proc. Natl. Acad. Sci. USA (1973) 73, 1761-1764). New aspects in relation to that study are the significantly increased EP and SP. In the classical EH model, based on obstruction of the absorptive function of the endolymphatic sac, increased SPs are accompanied by decreased EPs. In this cholera toxin model of EH, it is unlikely that the endolymphatic sac is involved. Apparently, EH can be based on mechanisms located in the cochlea itself as opposed to mechanisms located in the endolymphatic sac.

Animals↗
PubMed1985

Effects of sympathetic stimulation on the round window compound action potential in the rat.

The effect on the ear of stimulating the sympathetic nervous system was studied in rats by recording the compound action potentials (N1N2) in response to 2 kHz tonebursts presented to anesthetized rats before, during, and after electrical stimulation of the superior cervical ganglion, and evaluating the changes in N1 latency which resulted. Stimulation of the superior cervical ganglion was found to cause an increase in the N1 latency which was more pronounced at low stimulus intensities (mean value 0.09 +/- 0.04 ms (S.E.) at 5 dB above threshold) than at moderate stimulation intensities (0.08 +/- 0.04 ms at 15 dB above threshold), with little change in latency occurring at the highest intensity tested (0.02 +/- 0.01 ms at approximately 25-30 dB above threshold). In addition, individual animals varied in their responses to stimulation of the superior cervical ganglion, with some animals evidencing a great change in the latency of the response (0.4 ms increase at 10 dB above threshold) and others showing very little change in latency. This variability could not be related to the condition of the animal at the time of observation of the response. In one of the twelve animals there was a slight decrease in latency as a result of sympathetic stimulation (0.07 ms at 5 dB above threshold), and although not studied systematically, low frequencies seemed to be affected more than high frequencies. Further, the change in the amplitude of N1 was not systematically related to sympathetic stimulation. After the administration of hexamethonium (which blocks transmission in autonomic ganglia) in three rats there was no effect on the latency of the N1 potential from sympathetic stimulation as recorded before sympathetic stimulation.

Animals↗
PubMed1997

Decline in the endocochlear potential corresponds to decreased Na,K-ATPase activity in the lateral wall of quiet-aged gerbils.

The ion transport-mediating enzyme, Na,K-ATPase, is abundantly present in the cochlear lateral wall. This enzyme is essential for the generation and maintenance of the endocochlear potential. Diminished enzyme activity has been observed previously in the lateral wall of quiet-aged gerbils. The present study was designed to investigate the impact of the age-related decline in Na,K-ATPase specific activity upon auditory function. Measures of the resting endocochlear potential value and the level of Na,K-ATPase specific activity were made in cochleae obtained from gerbils aged in quiet conditions. Analysis revealed a high degree of correspondence between the level of lateral wall Na,K-ATPase specific activity and the value of the endocochlear potential measured in the round window/turn 1 region of the cochlea. Nonlinear regression models showed a strong relationship between the age-related reductions in enzyme activity and the magnitude of the endocochlear potential. The data suggest that during metabolic presbyacusis a decrease in Na,K-ATPase specific activity can explain most, but not all, of the decline in the endocochlear potential.

Aging↗
PubMed1998

Sarthran preserves cochlear microcirculation and reduces temporary threshold shifts after noise exposure.

The cause of noise-induced hearing loss remains unclear despite years of both epidemiologic and experimental investigation. Among the many possible pathophysiologic mechanisms that may contribute to noise-induced temporary or permanent threshold shifts are insufficiencies in cochlear blood flow. Although the literature is inconsistent, several histologic and physiologic studies demonstrate signs of reduced circulation in the cochlea after noise exposure. Recent studies using computer-enhanced intravital microscopy complement these earlier findings. Evidence suggests that these microcirculatory events are mediated in part by several circulating factors, including the potent vasoactive peptide angiotensin. This study investigated this possibility by pretreating with the angiotensin receptor antagonist sarthran during noise exposure and examining both cochlear microcirculation and auditory sensitivity. The results of these experiments show noise-induced ischemia in the lateral wall of the cochlea and temporary threshold shifts. Treatment with sarthran prevented this noise-induced microcirculatory ischemia and preserved auditory sensitivity at the low frequencies tested. These findings support a role for the angiotensinergic system during noise exposure and suggest that preservation of cochlear blood flow is functionally related to auditory sensitivity.

Acoustic Stimulation↗
PubMed1989

Arachidonate metabolites change furosemide-induced cochlear potentials.

Furosemide-induced changes of cochlear potentials were used as a model to study the influence of arachidonic acid metabolites on ion movements within the cochlea. No influence was exerted by the drugs Esculetin - blocking the synthesis of lipoxygenase products - and Dazoxiben - suppressing thromboxane A2 levels within the cochlea. A weakening of the furosemide-induced changes of the endocochlear potential was found when infusing the thromboxane (TX) receptor antagonists BM 13,505 and BM 13,177 before furosemide was given. This effect was also observed when pre-treating the guinea pig with a specific platelet-activating factor receptor antagonist, BN 52,021, before the diuretics was given. Summating potential and cochlear microphonics remained insignificantly changed against controls. The results suggest that a TX receptor contributes to the control of ion movements within the cochlea. A possible involvement of loop diuretics' receptors is discussed.

Acoustic Stimulation↗
PubMed1994

The effect of adenosine on cochlear potentials in the guinea pig.

The effect of adenosine on cochlear potentials was examined in the guinea pig. Perilymphatic perfusion with 10(-4) M adenosine produced a significant decrease in the amplitudes of cochlear microphonics, negative summating potential (-SP) and compound action potential (CAP) and significant prolongation of N1 latency with no change in the endocochlear potential. The decreases in the amplitudes of -SP and CAP caused by adenosine were dose-dependent. Perilymphatic perfusion with an inactive analogue, 8-bromoadenosine, produced no changes in the cochlear potentials. The A1-receptor agonist, 2-chloro-adenosine, produced a similar change in cochlear potentials to adenosine, while no changes were produced by the A2-receptor agonist, 5'-(N-ethylcarboxamido)-adenosine. These results suggest that adenosine may have a modulatory function through an A1 receptor in the cochlea.

2-Chloroadenosine↗
PubMed1992

[Experimental studies of ischemia of the cochlea. Part 1: Method].

For the etiology of certain inner ear diseases e.g. sudden hearing loss, an impaired cochlear blood flow is discussed. The model of the ferromagnetic thrombosis is an atraumatic method to produce a selective ischemia of the inner ear. The measurement of the inner ear potentials EP, MP and CAP can help to elucidate which inner ear structures are primarily impaired by local ischemia. During the action of a magnetic field to the right cochlea an intravenous injection of small iron particles leads to a thrombosis of the cochlear veins. EP, MP and CAP were measured in the thrombosed ear and MP and CAP in the undisturbed contralateral ear. The methods of microsurgery on the middle and inner ear, the electrophysiological measurement techniques of the inner ear potentials and the method of producing a ferromagnetic thrombosis are described in detail.

Animals↗