[Auditory evoked potentials and cochlear pathology].
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Aging↗
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A comparison of the effect of cochlear perfusion with ouabain on summating potentials and distortion product otoacoustic emissions in the guinea pig.
In order to investigate whether or not the summating potential (SP) and the 2f1-f2 distortion product otoacoustic emission (DPOAE) are due to related cochlear non-linearities, their behavior was studied in the guinea pig after intracochlear perfusion with ouabain and subsequent rinsing. The SP was evoked with either 4 or 8 kHz tone bursts, and the 2f1-f2 DPOAE was evoked with simultaneous presentations of 6.6 and 8 kHz continuous tones. After ouabain perfusion, DPOAE was dramatically reduced while the SP underwent only a small reduction. After rinsing out the ouabain with artificial perilymph, the DPOAE showed partial recovery while the SP displayed a large and long-lasting increase when compared to its a initial value. These results suggest that the non-linear processes giving rise to the SP and DPOAE are not identical.
Acoustic Stimulation↗
Time course of efferent fiber and spiral ganglion cell degeneration following complete hair cell loss in the chinchilla.
Ethacrynic acid (EA) is known to interact with aminoglycoside antibiotics such as gentamicin (GM). In the chinchilla, co-administration of GM and EA can produce hair cell lesions ranging from a small loss of outer hair cells (OHCs) in the base of the cochlea to complete destruction of all hair cells, depending on dosing parameters. Although hair cell loss has been characterized, little is known about the fate of efferent fibers or spiral ganglion neurons (SGNs) in this model. To study the time course of efferent fiber and SGN loss, chinchillas were injected with GM (125 mg/kg IM) followed immediately by EA (40 mg/kg IV). Estimates of efferent fiber loss and density changes were made after 3 days or 1, 2, 3, or 4 weeks of survival. Estimates of SGN loss and density changes were made after 15 days or 1, 2, 4, or 6 months of survival. Cochlear function was rapidly abolished and all cochlear hair cells were missing within 24 h after treatment. Inner hair cells (IHCs) in the middle turn of the cochlea died earlier than cells in the apex or base, and OHCs in Rows 1 and 2 died earlier than OHCs in Row 3. Degeneration of efferent nerve fibers began 3-7 days post-injection, versus 15-30 days for SGNs, and the loss of efferent fibers was essentially complete within 1 month, versus 2-4 months for SGNs. The rapid time course of efferent fiber and SGN loss in the chinchilla may make it a practical model for studying mechanisms of neural loss and survival in the mammalian inner ear.
Acetylcholinesterase↗
Electrically evoked compound action potentials of guinea pig and cat: responses to monopolar, monophasic stimulation.
We recorded electrically evoked compound action potentials (EAPs) from guinea pigs and cats using monophasic current pulses delivered by a monopolar intracochlear electrode. By using simple stimuli, we sought results that could shed light on basic excitation properties of the auditory nerve. In these acute experiments, the recording electrode was placed directly on the auditory nerve. Responses to anodic and cathodic stimulus pulses were recorded separately to evaluate stimulus polarity effects. Several polarity-dependent properties were observed. Both EAP morphology and latency were polarity-dependent, with greater latencies for cathodic stimulation. Threshold stimulus level was also polarity-dependent, but in different directions in the two species: cats had lower cathodic thresholds while guinea pigs had lower anodic thresholds. We also observed that the slopes of the EAP amplitude-level functions depended upon stimulus polarity. In most cases where EAP saturation amplitude could be measured, that amplitude was similar for anodic and cathodic stimuli, suggesting that either stimulus polarity can recruit all fibers, or at least a comparable numbers of fibers. The common findings (e.g., EAP morphology and polarity-dependent latency) observed in these two species suggest results that can be extrapolated to responses obtained in humans, while the species-specific findings (e.g., dependence of threshold on polarity) may point to underlying anatomical differences that caution against overgeneralization across species. Some of our observations also bear upon hypotheses of how electrical stimuli may excite different sites on auditory nerve fibers.
Action Potentials↗
The temperature dependency of neural and hair cell responses evoked by high frequencies.
A fine thermocouple, placed on the round window of the guinea pig cochlea, was used to measure temperature and electrical potentials. In acute experiments, rectal temperature was held constant at 38 degrees C while cochlear temperature was varied between 38 degrees C and 31.5 degrees C. Cochlear cooling to 36 degrees C caused elevated thresholds for the compound action potential (CAP) in response to tone bursts with frequencies above 24 kHz. CAP latencies increased for all frequencies tested (2 to 40 kHz). Cooling to lower temperatures produced larger latency increases and greater threshold shifts which extended to CAPs evoked by frequencies as low as 16 kHz. These CAP changes were fully reversible after a cochlear temperature of 38 degrees C was restored. In an attempt to create more uniform cooling of the cochlea, experiments were also conducted with round window thermo-couples chronically implanted in guinea pigs. After cooling the entire anesthetized animal to 36 degrees C, CAP thresholds were again elevated only for frequencies above 24 kHz. In other acute experiments, extracellular dc receptor potentials were recorded from the organ of Corti with micropipettes. Cooling caused a decreased sensitivity to tones at the characteristic frequency of the recording location (20 kHz) and had less effect on responses to lower frequencies. The receptor potential usually recovered after rewarming the cochlea. These data emphasize that temperature is an important parameter when electrophysiological measurements are being made. They also suggest an explanation for the reported discrepancy between behavioral and electrophysiological thresholds at high frequencies.
Action Potentials↗
Effect of iodoacetic acid upon cochlear potentials.
Lotz et al. reported that perilymphatic application of 5 X 10(-3) M iodoacetic acid (IAA) in the guinea pig does not influence the first-order cochlear microphonics (CM1) under aerobic conditions. However, in ischemia the rate of decline of the second-order microphonics (CM II, also called postmortem CM) was significantly increased by IAA. The authors concluded that glycolysis plays no role in maintaining the CMI, but that it is responsible for supporting the CMII. In carefully controlled experiments we found that in the respiring guinea pig, perilymphatic application of 5 X 10(-3) M IAA produced a rapid and pronounced effect upon both the endolymphatic potential and the CM. In particular, the CM dropped to less than 0.5% of its initial level within 40 min, due to IAA, whereas it took 120 min to drop to the same level in total ischemia (without IAA). We therefore reject the above-mentioned proposition that IAA is ineffective upon cochlear potentials under aerobic conditions; moreover, we find that even under aerobic conditions, the CM drops well below the usual CM II level substantially faster than under anaerobic conditions (without IAA). Other important findings, including an anoxia-sensitive negative component of the endolymphatic potential due to severe intoxication with IAA, and the effects of pretreatment of the organ of Corti with low concentrations of IAA upon the CM II are discussed.
Aerobiosis↗
Antagonistic action of reductants against vanadate-induced EP decrease.
The antagonistic action of ascorbic acid or glutathione against vanadate was studied by observing changes in EP in guinea pig cochlea. After intravenous injection of ascorbic acid or glutathione, the EP decrease induced by perfusion of the perilymphatic space with vanadate solution was suppressed and the EP showed a remarkable recovery in some animals. Intravenous preadministration of either of the two compounds inhibited or prevented the vanadate-induced EP decrease. When ascorbic acid or glutathione was added to the vanadate solution, the EP decrease was also inhibited. The chemical action of both reductants against vanadate is discussed. From the results obtained, it is speculated that a chemical balance between some oxidants and reductants in the stria vascularis, must be kept constant in order to maintain the EP at a constant potential level.
Animals↗
Evoked otoacoustic emissions and electrocochleography in a patient with multiple sclerosis.
A 24-year-old woman with multiple sclerosis had right-sided hearing impairment with tinnitus. She underwent electrocochleography (ECochG) and examination of evoked otoacoustic emissions (EOAEs) to assess cochlear function. An acoustic probe to measure EOAEs was inserted into the external ear canal. The ECochG action potential and cochlear microphonics were recorded by a transtympanic needle electrode technique. Both fast and slow components of EOAEs appeared in either the period of deteriorated hearing acuity or when it was improved. They showed normal detection thresholds and input-output curves during both periods. Cochlear microphonics with almost normal detection thresholds and input-output functions were obtained during the period of deteriorated hearing acuity. Action potential (N1) input-output curves during relapse with hearing loss were notably lower in amplitude and longer in latency than those obtained at the time hearing impairment showed improvement. The EOAE and ECochG findings suggested that this patient had almost normal cochlear function, and we assumed from the magnetic resonance imaging and auditory brain stem response findings as well as the ECochG that the hearing impairment was caused by dysfunction of auditory pathways in the brain stem, including structures that contribute to generation of the N1 potential of the ECochG.
Adult↗
Development of endocochlear potential and compound action potential in the rat.
The present study was designed to investigate the developmental changes of the endocochlear potential and compound action potential simultaneously from rat pups of various ages. Animals were anesthetized with ketamine/xylazine, and the endocochlear potential was measured with a glass microelectrode. At the same time, a wire electrode was placed on the round window to record the click-evoked compound action potential. The endocochlear potential was found to be very low during the first few days of postnatal life. A rapid increase in the value of the endocochlear potential was noted between eleven and thirteen days of age, and adult-like values were recorded by seventeen days of age. Compound action potential responses were recorded at thirteen days of age to high intensity clicks, followed by a progressive improvement of thresholds and reduction of latencies. The development of the endocochlear potential and compound action potential was found to be reciprocally related - as the magnitude of the endocochlear potential increased, the compound action potential threshold declined with increasing age. The development of the endocochlear potential was found to closely approximate the development of enzymatic activity of sodium, potassium-ATPase in the stria vascularis reported by Kuijpers (1974).
Action Potentials↗
Systemic co-treatment with alpha-melanocyte stimulating hormone delays hearing loss caused by local cisplatin administration in guinea pigs.
It has previously been demonstrated that ototoxicity induced by systemic administration of cisplatin is reduced by concomitant administration of melanocortins, like alpha-melanocyte stimulating hormone (alpha-MSH). However, these experiments were hampered by large interanimal variability. Therefore, we re-investigated the effects of systemically administered alpha-MSH during local (intracochlear) administration of cisplatin. Guinea pigs, implanted with a round-window electrode, allowing daily monitoring of the compound action potentials (CAPs), and a mini-osmotic pump, pumping either 0.5 microl/h physiological saline or cisplatin solution (15 microg/ml), were co-treated daily with a subcutaneous bolus injection of either alpha-MSH (75 microg/kg) or physiological saline for 1 week or until the electrocochleogram showed a persistent decrease in CAP amplitude (40 dB threshold shift at 8 kHz). Next, the animals were sacrificed and the cochleas were processed for histology. After 2-3 days, cisplatin alone caused a threshold shift at all frequencies (2-16 kHz). Co-administration with alpha-MSH consistently delayed the criterion threshold shift by 1 day. When the 40 dB criterion had been reached, similar outer hair cell losses in both the cisplatin/alpha-MSH- and cisplatin/saline-treated groups were observed. This experiment confirms that direct administration of cisplatin into the cochlea results in considerably less interanimal variability than systemic administration and that co-treatment with alpha-MSH delays cisplatin ototoxicity. Since cisplatin was delivered directly to the cochlea, the ameliorating effect of alpha-MSH probably involves a cochlear target.
Action Potentials↗
Disruption of cochlear potentials by chemical asphyxiants. Cyanide and carbon monoxide.
While ischemia, hypoxic hypoxia, and carbon monoxide (CO) have received extensive study designed to characterize mechanisms by which they disrupt cochlear function, little data are available concerning cyanide's potential to disrupt auditory function. In this study, disruption of the compound action potential (CAP) and endocochlear potential (EP) by cyanide and CO was compared in rats treated with potassium cyanide (KCN) (7 mg/kg ip), saline, CO (35 ml/kg ip), and air. Acute KCN administration significantly suppressed CAP and EP transiently. The effect was seen initially on EP with CAP impairment occurring a few minutes later. Acute CO injection also suppressed the CAP significantly, but the effect was far smaller, occurred later in time, and lasted longer than the effect of KCN. The effect of CO on EP was equivocal. There was a good correspondence between blood cyanide levels and impairment of cochlear function; carboxyhemoglobin (HbCO) levels were elevated during the period when cochlear function was impaired, but recovery of cochlear function preceded the return of normal oxyhemoglobin. Both KCN and CO had somewhat preferential effects on high-frequency tones. Repeated cyanide administration caused a persistent CAP threshold elevation despite the rapid recovery of EP and CAP observed following acute KCN administration. The data suggest that acute KCN administration has a prominent disruptive effect at the stria vascularis presumably by disrupting the electron transport chain in this metabolically active structure. The principal target for acute CO ototoxicity in the cochlea is probably not the stria vascularis.
Action Potentials↗
[Protective properties of nicotinamide and cytochrome C in aminoglycoside ototoxicosis].
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Action Potentials↗
[Potassium ion secretion and generation of the endocochlear potential in the stria vascularis].
Central to inner ear research are questions regarding the homeostasis of the high endolymphatic potassium concentration (approximately 150 mmol/l) and the high endocochlear potential (approximately +80 mV). Disturbances of the endocochlear potential can lead to the immediate loss of hearing which may be irreversible. The molecular mechanism leading to the generation of the endocochlear potential has not yet been discovered in spite of its clinical relevance. It is long known, however, that the stria vascularis is responsible for both the generation of the endocochlear potential as well as the secretion of potassium into endolymph. Recent investigations have clarified the mechanisms leading to the secretion of potassium and have led to the formulation of a now widely accepted model. This model explaining potassium secretion as well as the generation of the endocochlear potential is discussed in the present article.
Animals↗
An electrophysiologic study of experimental perilymphatic fistula.
This study was undertaken to elucidate the mechanism that causes sensorineural hearing loss in clinical cases with perilymphatic fistula. Perilymph was experimentally aspirated through the round window membrane in 17 guinea pigs. The extent of cochlear damage was examined electrophysiologically as well as histopathologically. Immediately after aspiration, several types of changes in summating potential (SP) were observed. Two animals without a polarity change of the SP showed only slight threshold changes in both cochlear microphonic and action potentials, and no specific histopathologic changes in the cochlea. Reversed polarity of the SP was observed in three animals, of which one showed a high-amplitude negative SP followed by rapidly progressive hearing loss. Bulging of Reissner's membrane was confirmed histopathologically in this case. The SP disappeared in the remaining 12 animals. In animals with profound electrophysiologic changes, bulging or rupture of Reissner's membrane and damaged hair cells were observed. These findings suggest that an abrupt change in perilymphatic pressure produces morphologic changes in the membranous labyrinth, causing changes in the vibration function of the cochlear partition and in the function of the organ of Corti. Abrupt pressure imbalance may be a causative factor of sensorineural hearing loss in the case of perilymphatic fistula.
Acoustic Stimulation↗
Electrophysiological and morphological evaluation of the acute ototoxicity of sodium nitroprusside.
Nitric oxide (NO) is a messenger molecule that mediates several physiological functions and pathological processes. Sodium nitroprusside (SNP), a potent vasodilator, when given clinically as an anti-hypertension agent, exerts its function by releasing NO. It was reported recently that SNP causes a loss of auditory nerve compound action potential (CAP) after topical application of SNP on guinea pig round window membrane (RWM). The current study was designed to investigate the ototoxic target of SNP through both electrophysiological and morphological approaches. The CAP threshold at frequencies ranging from 2 to 36 kHz, the cochlear microphonic quadratic distortion product (cmQDP, F2-F1, where F1 = 17.1 kHz; F2 = 18 kHz), and the cochlear microphonic (CM) at the frequency of F1 were recorded via a round window electrode before and up to 2 h after RWM application of 1 microliter of drug solution. Cochlear blood flow (CBF) and arterial blood pressure were monitored. The cochleae were then processed for morphological examination. The effect of SNP on endocochlear potential (EP) was also studied. Results showed that cmQDP, CM, and CAP, as well as EP, were suppressed in varying amounts, while CBF was substantially increased following drug application. Morphological evaluations showed swelling of the afferent inner radial dendrites within the basal cochlear turn in the higher concentration groups of SNP, while the hair cells presented no evidence of damage at the light microscopic level. The results indicate that SNP has an acute ototoxic effect in a concentration- and time-dependent manner. The targets of SNP ototoxicity are at least the afferent dendrites and stria vascularis.
Action Potentials↗
The Goldman-Hodgkin-Katz equation and graphical 'load-line' analysis of ionic flow through outer hair cells.
While the 'membrane potential' of a cell which has a homogeneous membrane and surrounding environment, and which is not pumping ions electrogenically (passing no net current through its membranes), can be estimated from the Goldman voltage equation, this equation is inappropriate for other cells. In the mammalian cochlea such problematic cells include the cells of stria vascularis and the sensory hair cells of the organ of Corti. Not only is the Goldman voltage equation inappropriate, but in asymmetric cells the concept of a single 'membrane potential' is misleading: a different transmembrane voltage is required to define the electrical state of each section of the cell's heterogeneous membrane. This paper presents a graphical 'load-line analysis' of currents through one such asymmetric cell, the outer hair cells of the organ of Corti. The approach is extremely useful in discussing the effects of various cochlear manipulations on the electrical potential within hair cells, even without a detailed knowledge of their membrane conductance. The paper discusses how modified Goldman-Hodgkin-Katz equations can be used to describe stretch-activated channels, voltage-controlled channels, ligand-mediated channels, and how the combination of these channels and the extracellular ionic concentrations should affect the hair cell's resting intracellular potential and resting transcellular current, its receptor current and receptor potential, and the extracellular microphonic potential around these cells. Two other issues discussed are the role of voltage-controlled channels in genetically determining membrane potential, and the insensitivity of hair cells to changes of extracellular potassium concentration under some conditions.
Acoustic Stimulation↗
[A basic study of summating potential (ECoG) with tone burst].
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Acoustic Stimulation↗
Modulation of cochlear responses in the guinea pig by low-frequency, phase-shifted maskers following noise trauma.
Low-frequency acoustic biasing using an intensive phase-shifted, low-frequency masker was studied according to its ability to determine disorders of cochlear micromechanics following noise trauma in the guinea pig as animal model. Statistical analyses proved that this technique allowed electrophysiological differentiation of controls versus groups with different degrees of experimentally induced threshold shifts. To substantiate group differences an intensity of at least 70 dB SPL was required for the 52 Hz masker and the difference in relation to the test-tone intensity had to be +/- 10 or +/- 20 dB SPL. The noise-traumatized cochlea could be identified by means of a threshold shift for the 5 microV pseudothreshold, a low modulation span of the compound action potential amplitude (< 25-50 microV frequency dependent), and reduced positive summating potential amplitude with negative non-modulating values within the different measurement phases for 1 and 2 kHz stimulation.
Acoustic Stimulation↗