Deise Lima da Costa ,
Anne Chibois ,
Jean-Paul Erre ,
Christophe Blanchet ,
RENAUD CHARLET de Sauvage , and
Jean-Marie Aran
Laboratoire d'Audiologie Expérimentale et Clinique, Unité Propre de ...Recherche-Enseijnement Supérieur Université de Bordeaux II, Hôpital Pellegrin, 33076 Bordeaux, France
Lima da Costa, Deise, Anne Chibois, Jean-Paul Erre, Christophe Blanchet, Renaud Charlet de Sauvage, and Jean-Marie Aran. Fast, slow, and steady-state effects of contralateral acoustic activation of the medial olivocochlear efferent system in awake guinea pigs: action of gentamicin. J. Neurophysiol. 78: 1826-1836, 1997. The function of the medial olivocochlear efferent system was observed in awake guinea pigs by recording, in the absence of ipsilateral external acoustic stimulation, the ensemble background activity (EBA) of the VIIIth nerve from an electrode chronically implanted on the round window of one ear. The EBA was measured by calculating the power value of the round window signal in the 0.5- to 2.5-kHz band after digital or analog (active) filtering. This EBA was compared with and without the addition of a low-level broadband noise to the opposite ear. The contralateral broadband noise (CLBN, 55 dB SPL) induced, via the efferent system, a decrease (suppression) of this EBA. With the use of noise bursts of different durations, two components in this suppression could be observed. After the onset of a 1-s CLBN, the power value of the EBA decreased rapidly by 38.0 ± 4.2% (mean ± SD, n = 3), with a latency of <10 ms and a decay time constant of 13.1 ± 1.0 ms (fast effect). At the offset of the 1-s CLBN, EBA came back to prestimulation values with a similar latency and a time constant of 15.5 ± 2.9 ms. During longer CLBN stimulation ( 1 min), EBA presented, after the fast decrease, an additional, slower decrease of 15.6 ± 3.1%, with a delay of 9.8 ± 1.3 s and a decay time constant of 16.1 ± 5.0 s ( n = 12, slow effect), and then remained remarkably constant for as long as observed, i.e., >2 h (steady state). The average global suppression was thus up to 47.8 ± 5.8% of the basal, pre-CLBN-stimulation EBA value. At the offset of the CLBN, EBA returned to pre-CLBN level with fast and slow phases, with, for the slow phase, no delay and a time constant of 32.1 ± 8.1 s. Fast and slow changes in EBA power values were observed after a single injection of gentamicin (GM) at different doses (150, 200, and 250 mg/kg). At 150 and 200 mg/kg, GM progressively and reversibly blocked the rapid effect, but the slow component of the efferent medial suppression remained remarkably unchanged. However, at higher doses both the fast and slow suppressions were totally yet still reversibly blocked. These observations indicate that the medial olivocochlear efferent system exerts sustained influences on outer hair cells and that this effect develops in two different steps that may have different basic cellular mechanisms.
The bioelectrical activity of the cochlea, without any ipsilateral acoustic stimulation, was recorded in awake guinea pigs (GPs) between electrodes chronically implanted at the round window (RW) and ...the skull. Measuring its power in the band centered around 1.0 kHz (0.5-2.5 kHz) provided an indirect measure of the ensemble background (EBA) activity of the eighth nerve. Contralateral white-noise (CLWN) stimulation reduced this EBA, presumably by activation of medial olivocochlear fibers. The aim of the investigation was to validate measurements of EBA and of its contralateral suppression in order to study the medial efferent function. The first goal was to find the best conditions for recording the EBA in the absence of ipsilateral stimulation and for studying its suppression by contralateral acoustic stimulation, which implies that no noise was generated by the experimental animal. Thus recordings were compared in normal, awake GPs and in GPs under sedation with xylazine, anesthetized with a combination of xylazine and ketamine, and with and without temperature regulation. In order to monitor the effects of sedation and anesthesia, the recordings were analyzed not only in the 0.5- to 2.5-kHz frequency band but also in the other frequency bands, 5-50 Hz, 50-150 Hz, and 150-500 Hz, which presumably include general central and neuromuscular contributions. The results show that sedation with xylazine accompanied by regulation of body temperature does not affect the EBA value nor its contralateral suppression. Nevertheless, anesthesia should be avoided, even with control of body temperature. The second goal of this study was to identify the specific cochlear contribution to the raw RW signal. Thus recordings were performed in normal and deafened animals and analyzed in the frequency band 0.5-2.5 kHz and also in the other frequency bands of 5-50 Hz, 50-150 Hz, and 150-500 Hz. The results indicate that most of the cochlear activity lies in the frequency band 0.5-2.5 kHz, with also some minor contribution coming from the 150- to 500-Hz band. Analysis and comparison of power values in the different conditions indicate that specific cochlear EBA power was about 60 microV2. From a commonly accepted mean background discharge rate of 50 spikes/s (sp/s), the EBA power without CLWN should have been around 4.4 microV2 if the fibers' activity was random. This difference suggests that there is probably some degree of synchrony between individual fibers. There was a reduction of approximately 45% during CLWN stimulation. This suppression might correspond to a reduction in both discharge rate and synchrony of the fibers.
The influence of xylazine on the amplitude, latency and waveform of VIIIth nerve compound action potential (CAP) and cochlear microphonic (CM) in response to clicks at 95 dB SPL in normal awake ...preimplanted guinea pigs was investigated. The animals' temperature was monitored but no thermoregulation was exerted, except in one control experiment. Following a 0.2 ml injection of xylazine, CM showed minor variations while CAP audiograms for tone pips between 0.5 and 25 kHz remained normal. However, a progressive decrease in temperature and a strongly correlated increase in CAP amplitude and in N1 and N2 latencies were noticed. For peak N1 the changes were equivalent to linear amplitude and time expansions, and could be reproduced through CAP synthesis with convolution methods using time expanded unit response model and firing density functions. All changes were maximal after 2 h of sedation and recovered within approximately another 2 h. Whereas xylazine is known to induce hypothermia, all the changes disappeared if the animal was thermoregulated. Therefore the changes are interpreted as a result of hypothermia. The mechanism of N1 latency lengthening and increase in amplitude during hypothermia can be understood as a simultaneous increase in spike duration, hair cell/nerve synaptic delay and postsynaptic time constant. This hypothesis yielded a theoretical temperature coefficient for N1 latency (−52 μs/°C) matching that measured experimentally (−55 μs/°C). When compared with peak N1, peak N2 appeared relatively more expanded. Arguments about the origin of N2 are discussed.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
There is some evidence from epidemiological studies of an association between occupational exposure to electromagnetic fields and Amyotrophic Lateral Sclerosis (ALS). Our aim was to perform, for the ...first time, an animal study in a controlled magnetic environment. We used the SOD-1 mouse model to assess the possible effect of ELF magnetic fields on development of the disease. Seven mice per group were exposed to 50 Hz magnetic fields at two intensities (100 and 1000 µTrms) before the onset of the clinical signs of ALS. Exposure lasted 7 weeks, and body weight, motor performance and life span were monitored. Our results did not reveal any evidence of a link between ELF exposure and ALS in this transgenic animal model.
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DOBA, IJS, IZUM, KILJ, NUK, PILJ, PNG, SAZU, UILJ, UKNU, UL, UM, UPUK
Contralateral broadband noise (BBN) elevates ipsilateral auditory thresholds (central masking) and reduces the amplitude of ipsilateral brainstem auditory evoked potentials (BAEPs). Binaural ...interactions are complex psychophysical phenomena, but binaural interaction components are easily extracted from BAEPs to monaural versus binaural click stimulation. However, contralateral, or binaural, acoustical stimulation is known to activate simultaneously the crossed and uncrossed medial olivocochlear (MOC) efferent systems and decrease activity in both cochleas. Particularly, contralateral BBN stimulation suppresses in part ipsilateral peripheral activity. What is the role of such contralateral induced peripheral suppression in the overall changes in central BAEPs observed during contralateral masking or binaural stimulation? Compound action potentials (CAPs) of the auditory nerve and BAEPs were recorded simultaneously in awake guinea pigs from electrodes chronically implanted on the round window of the cochlea and the surface of the brain. Peripheral and central measures of contralateral masking and binaural interactions were obtained from responses to monaural or binaural clicks, with or without contralateral BBN, recorded before, during, and after the reversible blockade of the MOC function following a single intramuscular injection of gentamicin. Contralateral BBN effectively reduced the amplitudes of CAP and of all BAEP peaks. CAP to ipsilateral click did not, however, change significantly from monaural to binaural click stimulation; still, normal binaural interaction components developed in the BAEPs. When the medial efferent function was blocked by gentamicin, the normal contralateral BBN suppression of CAP and of the earliest BAEP peak was lost; however, the later BAEP peaks were suppressed by contralateral BBN as before gentamicin, and the central binaural interaction components were unchanged. In these experimental conditions, the MOC efferent system seems to play little role in centrally recorded contralateral masking and binaural interactions.
Sumario
El ruido de banda ancha (BBN) eleva los umbrales auditivos ipsilaterales (enmascaramiento central) y reduce la amplitud de los potenciales auditivos evo-cados (BAEPs) ipsilaterales. La interacción es un fenómeno psicofísico complejo, pero los componentes de interacción binaural pueden ser extraídos fácilmente de los BAEPs al estimular con clicks uno vs ambos oídos. Sin embargo, se sabe que la estimulación acústica contralateral y la binaural activan simultáneamente el sistema olivo-coclear medial (MOC) cruzado o ipsilateral y disminuyen la activi-dad de las dos cócleas. La estimulación con BBN particularmente suprime en parte la actividad per-iférica Cuál sería el papel de esa supresión per-iférica inducida, en los cambios en los BAEPs centrales observados durante el enmascaramiento contralateral o la estimulación binaural? Se regis-traron simultáneamente los componentes de los potenciales de acción (CAPs) del nervio auditivo y los BAEPs en conejillos de Indias despiertos a través de electrodos implantados en la ventana redonda y en la superficie del cerebro. Se obtuvieron mediciones del enmascaramiento contralateral periférico y central y de las interacciones binaurales ante estímulos mono o binaurales con clicks, con o sin BBN contralateral; antes durante o después del bloqueo reversible de la función del MOC con una aplicación única intramuscular de Gentamicina. El BBN contralateral redujo la amplitud de los CAPs y de todos los picos de BAEPs. Los CAPs con clicks ipsilaterales no se modificaron significativamente al estimular con clicks monoaurales o binaurales, pero si desarrollaron componentes de interacción binaural en los BAEPs. Cuando se bloqueó la función eferente medial con Gentamicina se perdió tanto la supresión de los CAPs contralaterales con BBN, como los picos iniciales de los BAEPs; sin emabargo, se suprimieron los BAEPs tardfos con BBN contralateral como antes de la Gentamicina y los componentes de la interacción binaural central permaneció sin cambios. En estas condiciones experimentales, el MOC parece tener un papel mínimo en el enmascaramiento central y en las interacciones binaurales.
In the electrical stimulation (ES) of auditory pathways, the type of stimulus and the electrode/tissue interface are critical parameters for the safety and efficacy of the protocol. In this study the ...influence of alternate pulses, applied between round window and vertex electrodes in chronically implanted guinea pigs, and maintained during 1 and 25 daily periods of 2 h (short-term and long-term experiments, respectively), was investigated. ES consisted of monophasic current pulses of ±70 μA and 300 μs in duration at a rate of 167/s, with alternate polarity. Compound Action Potential (CAP) audiograms, amplitudes and latencies of click-evoked CAPs, amplitudes and latencies of electrically-evoked auditory responses (EARs), and electrode impedances, were measured periodically outside or during the ES periods. Short-term ES induced no change in CAP thresholds, amplitude and latency in response to clicks at 80 dB above normal threshold, but induced a slight latency increase and amplitude decrease of the EAR, correlated with an exponential decay of the electrode impedance. On a long-term basis, CAP audiograms and latencies did not change significantly, whereas CAP amplitudes and electrode impedances increased, in correlation with each other. In control guinea pigs receiving no ES, the same CAP amplitude and impedance changes were observed over the same long-term period. The EAR and CAP changes can be explained by a variation of the electrical impedance of the electrode/tissue interface. This is possibly due to a change in electrotytes around the electrode under the influence of the ES for the short-term variation, and to an electrode encapsulation by fibrous tissue independent of the ES for the long-term change. In itself, and under the conditions of this experiment, the ES demonstrated no adverse effects on the auditory function and can be safely used for inner-ear exploration.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
The purpose of this study was to evaluate the average discharge rate of all fibres in the whole auditory nerve (
R
wn) when a broad-band noise with steady-state effects is applied to the ear. We ...assessed the
R
wn parameter by detecting the state of refractoriness of the nerve during noise stimulation using an electric stimulus (ES) as a probe. The technique, applied in awake pre-implanted guinea pigs (Charlet de Sauvage et al., 1994), made it possible to obtain electro-acoustic responses (EARs), from which an estimate of the
R
wn parameter could be deduced. Negative current pulses of 100 μs duration, each followed by an identical pulse of positive polarity for charge balance, were applied between round window and indifferent vertex electrodes at intervals of 160 ms. The 120 ms wide-band noise masker started 92 ms before every other negative ES. The signal on the stimulating electrodes was averaged over a 5.12 ms window in synchrony with the negative pulse. EARs were obtained by alternately subtracting recordings during noise from those during silence. The
R
wn parameter was determined by comparing experimental and computed EAR patterns. For this purpose, a model of unit response incorporating changes in amplitude and conduction velocity during the relative refractory period was designed. The recovery function of the firing probability in response to ES was evaluated. Fibres were classified in different categories according to their background discharge rates. The probability of response of single fibres to ES in each category was calculated on the basis of their interval histograms during silence and noise. Individual spikes were combined accordingly to obtain the computed EAR waveform.
R
wn was determined by adjusting the EAR amplitude of the model in relation to that of the experimental EAR.
R
wn generally increases in a linear fashion with respect to noise intensity expressed in dB, thus following the increase in loudness perception estimated by Weber’s law. At the highest noise levels,
R
wn tends to saturate. The estimated saturation rate was found to be about 380 spikes/s.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
An experimental study of the electrical stimulation of the guinea pig cochlea is made using an electrode on the round window for both stimulation and recording. The neural response is separated from ...the electrical artifact with a masking procedure combined with a low amplification, "statistical" averaging method Charlet de Sauvage et al., Hear. Res. 2, 343-346 (1980). The high electrical impedance required for recording physiological responses implies the use of a current pulse generator. Monitoring of evoked potentials from the auditory cortex provides evidence that the effects of electrical stimulation (and of masking noise) are of auditory origin. The electrically evoked round window response is of very short latency (less than 0.2 ms). There is a response threshold for both electrical stimulus and masking noise. The response amplitude varies monotonically as a function of masking noise or electrical stimulus intensity. Experiments with high-pass noise masking suggest that the electrical stimulus is mainly acting on basal fibers. The response latency and waveform are independent of electrical stimulus intensity, repetition rate, masker level, or spectrum. Little intersubject variation is noted. Our experiments (reciprocal forward masking by electrical and acoustic stimuli) suggest that a direct, instantaneous electrical stimulation of the fibers occurs. We believe that this response to electrical stimulation represents the mean unit response of the auditory nerve fibers. This approach may be useful in the separate study of cochlear and VIIIth nerve functions and in the analysis (deconvolution) of the acoustically evoked compound AP.
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