Middle Ear Muscle Contractions Research Articles

Vocalization-induced middle ear muscle reflex and auditory fovea do not contribute to the unimpaired auditory sensitivity after intense noise exposure in the CF-FM bat, Hipposideros pratti.

Behaviors and auditory physiological responses of some species of echolocating bats remain unaffected after exposure to intense noise, but information on the underlying mechanisms remains limited. Here, we studied whether the vocalization-induced middle ear muscle (MEM) contractions (MEM reflex) and auditory fovea contributed to the unimpaired auditory sensitivity of constant frequency-frequency modulation (CF-FM) bats after exposure to broad-band intense noise. The vocalizations of the CF-FM bat, Hipposideros pratti, were inhibited through anesthesia to eliminate the vocalization-induced MEM reflex. First, the anesthetized bats were exposed to intense broad-band noise, and the findings showed that the bats could still maintain their auditory sensitivities. However, auditory sensitivities were seriously impaired in CBA/Ca mice exposed to intense noise under anesthesia. This indicated that the unimpaired auditory sensitivity in H. pratti after exposure to intense noise under anesthesia was not due to anesthetization. The bats were further exposed to low-frequency band-limited noise, whose passband did not overlap with echolocation call frequencies. The results showed that the auditory responses to sound frequencies within the noise spectrum and one-half octave higher than the spectrum were also unimpaired. Taken together, the results indicate that both vocalization-induced MEM reflex and auditory fovea do not contribute to the unimpaired auditory sensitivity in H. pratti after exposure to intense noise. The possible mechanisms underlying the unimpaired auditory sensitivity after echolocating bats were exposed to intense noise are discussed.

Effects of unilateral eye closure on middle ear muscle contractions

Middle ear muscle contractions (MEMCs) are most commonly considered a response to high-level acoustic stimuli. However, MEMCs have also been observed in the absence of sound, either as a response to somatosensory stimulation or in concert with other motor activity. The relationship between MEMCs and non-acoustic sources is unclear. This study examined associations between measures of voluntary unilateral eye closure and impedance-based measures indicative of middle ear muscle activity while controlling for demographic and clinical factors in a large group of participants (N=190) with present clinical acoustic reflexes and no evidence of auditory dysfunction. Participants were instructed to voluntarily close the eye ipsilateral to the ear canal containing a detection probe at three levels of effort. Orbicularis oculi muscle activity was measured using surface electromyography. Middle ear muscle activity was inferred from changes in total energy reflected in the ear canal using a filtered (0.2 to 8 kHz) click train. Results revealed that middle ear muscle activity was positively associated with eye muscle activity. MEMC occurrence rates for eye closure observed in this study were generally higher than previously published rates for high-level brief acoustic stimuli in the same participant pool suggesting that motor activity may be a more reliable elicitor of MEMCs than acoustic stimuli. These results suggest motor activity can serve as a confounding factor for auditory exposure studies as well as complicate the interpretation of any impulsive noise damage risk criteria that assume MEMCs serve as a consistent, uniform protective factor. The mechanism linking eye and middle ear muscle activity is not understood and is an avenue for future research.

Exploring the middle ear function in patients with a cluster of symptoms including tinnitus, hyperacusis, ear fullness and/or pain

Middle ear muscle (MEM) abnormalities have been proposed to be involved in the development of ear-related symptoms such as tinnitus, hyperacusis, ear fullness, dizziness and/or otalgia. This cluster of symptoms have been called the Tonic Tensor Tympani Syndrome (TTTS) because of the supposed involvement of the tensor tympani muscle (TTM). However, the putative link between MEM dysfunction and the symptoms has not been proven yet and the detailed mechanisms (the causal chain) of TTTS are still elusive. It has been speculated that sudden loud sound (acoustic shock) may impair the functioning of the MEM, specifically the TTM, after an excessive contraction. This would result in inflammatory processes, activation of the trigeminal nerve and a change of the MEMs state into a hypersensitive one, that may be associated to the cluster of symptoms listed above. The goal of this study is to provide further insights into the mechanisms of TTTS. The middle ear function of 11 patients who reported TTTS symptoms has been investigated using either admittancemetry and/or measurement of air pressure in the sealed external auditory canal. While the former method measured the middle ear stiffness the latter provides an estimate of the tympanic membrane displacement. Most patients displayed results consistent with phasic contractions of the TTM (n = 9) and/or Eustachian Tube (ET) dysfunction (n = 6). The MEM contraction or ET dysfunction could be evoked by acoustic stimulation (n = 3), somatic maneuvers (n = 3), or pressure changes in the ear canal (n = 3). Spontaneous TTM contraction (n = 1) or ET opening (n = 1) could also be observed. Finally, voluntary contraction of MEM was also reported (n = 5). On the other hand, tonic contraction of the TTM could not be observed in any patient. The implications of these results for the mechanisms of TTTS are discussed.

Contraction of the stapedius and tensor tympani muscles explored by tympanometry and pressure measurement in the external auditory canal

It has been suggested that tensor tympani muscle (TTM) contraction may be involved in the development of ear-related pathologies such as tinnitus, hyperacusis and otalgia, called the tonic tensor tympani syndrome (TTTS). However, as there is no precise measure of TTM function under normal and pathological states, its involvement remains speculative. When the TTM or the stapedius muscle (SM) contracts, they both generate an increase of middle ear stiffness that can be measured through middle ear admittance. However, this technique cannot differentiate the contraction between the two muscles. On the other hand, the air pressure measured in a sealed external auditory canal can provide a measure of the eardrum displacement that may be able to differentiate SM from TTM contraction. TTM is attached to the malleus, and its contraction causes a retraction of the eardrum inside the middle ear cavity, while SM can have a small but reversed effect on TTM displacement. To investigate this issue, we compared the middle ear admittance and air pressure in a sealed external ear canal upon auditory stimulation (sMEMC) and voluntary middle ear muscle contraction (vMEMC). In addition, we assessed the perceptual effect of vMEMC, including pitch and loudness matching of the fluttering noise produced by vMEMC and the threshold shifts, were measured. Out of the 14 ears tested, sMEMC was associated with a decrease of admittance in 93% (mean peak average: -0.06 ml, SD:0.04) and an increase of air pressure in 29% of ears (mean peak average: 8.1 Pa, SD:5.1). No decrease in air pressure was found upon sMEMC. For vMEMC (n = 8 ears), decreases were found for both admittance and air pressure in 100% and 88%, with a mean peak average of -0.38 ml, SD: 0.54 and -149 Pa, SD:156, for admittance and pressure respectively. These results suggest that SM and TTM are involved in sMEMC and vMEMC, respectively. In addition, vMEMC was associated with perceptual effects including a low-frequency sound, pitch-matched at ∼30 Hz (>15 dB SL), and a low-frequency hearing loss of at least 10 dB between 20 and 200 Hz. In conclusion, admittance and air pressure recordings provide useful and complementary information on middle ear muscle contraction and can be used to explore the middle ear function.

Generalizability of clinically measured acoustic reflexes to brief sounds.

Middle ear muscle contractions (MEMC) can be elicited in response to high-level sounds, and have been used clinically as acoustic reflexes (ARs) during evaluations of auditory system integrity. The results of clinical AR evaluations do not necessarily generalize to different signal types or durations. The purpose of this study was to evaluate the likelihood of observing MEMC in response to brief sound stimuli (tones, recorded gunshots, noise) in adult participants (N = 190) exhibiting clinical ARs and excellent hearing sensitivity. Results revealed that the presence of clinical ARs was not a sufficient indication that listeners will also exhibit MEMC for brief sounds. Detection rates varied across stimulus types between approximately 20% and 80%. Probabilities of observing MEMC also differed by clinical AR magnitude and latency, and declined over the period of minutes during the course of the MEMC measurement series. These results provide no support for the inclusion of MEMC as a protective factor in damage-risk criteria for impulsive noises, and the limited predictability of whether a given individual will exhibit MEMC in response to a brief sound indicates a need to measure and control for MEMC in studies evaluating pharmaceutical interventions for hearing loss.

Effect of Probe-Tone Frequency on Ipsilateral and Contralateral Electrical Stapedius Reflex Measurement in Children With Cochlear Implants.

The upper loudness limit of electrical stimulation in cochlear implant patients is sometimes set using electrically elicited stapedius reflex thresholds (eSRTs), especially in children for whom reporting skills may be limited. In unilateral cochlear implant patients, eSRT levels are measured typically in the contralateral unimplanted ear because the ability to measure eSRTs in the implanted ear is likely to be limited due to the cochlear implant surgery and consequential changes in middle ear dynamics. This practice is particularly limiting in the case of fitting bilaterally implanted pediatric cases because there is no unimplanted ear option to choose for eSRT measurement. The goal of this study was to identify an improved measurement protocol to increase the success of eSRT measurement in ipsilateral or contralateral or both implanted ears of pediatric cochlear implant recipients. This work hypothesizes that use of a higher probe frequency (e.g., 1000 Hz compared with the 226 Hz standard), which is closer to the mechanical middle ear resonant frequency, may be more effective in measuring middle ear muscle contraction in either ear. In the present study, eSRTs were measured using multiple probe frequencies (226, 678, and 1000 Hz) in the ipsilateral and contralateral ears of 19 children with unilateral Advanced Bionics (AB) cochlear implants (mean age = 8.6 years, SD = 2.29). An integrated middle ear analyzer designed by AB was used to elicit and detect stapedius reflexes and assign eSRT levels. In the integrated middle ear analyzer system, an Interacoustics Titan middle ear analyzer was used to perform middle ear measurements in synchrony with research software running on an AB Neptune speech processor, which controlled the delivery of electrical pulse trains at varying levels to the test subject. Changes in middle ear acoustic admittance following an electrical pulse train stimulus indicated the occurrence of an electrically elicited stapedius reflex. Of the 19 ears tested, ipsilateral eSRTs were successfully measured in 3 (16%), 4 (21%), and 7 (37%) ears using probe tones of 226, 678, and 1000 Hz, respectively. Contralateral eSRT levels were measured in 11 (58%), 13 (68%), and 13 (68%) ears using the three different probe frequencies, respectively. A significant difference was found in the incidence of successful eSRT measurement as a function of probe frequency in the ipsilateral ears with the greatest pair-wise difference between the 226 and 1000 Hz probe. A significant increase in contralateral eSRT measurement success as a function of probe frequency was not found. These findings are consistent with the idea that changes in middle ear mechanics, secondary to cochlear implant surgery, may interfere with the detection of stapedius muscle contraction in the ipsilateral middle ear. The best logistic, mixed-effects model of the occurrence of successful eSRT measures included ear of measurement and probe frequency as significant fixed effects. No significant differences in average eSRT levels were observed across ipsilateral and contralateral measurements or as a function of probe frequency. Typically, measurement of stapedius reflexes is less successful in the implanted ears of cochlear implant recipients compared with measurements in the contralateral, unimplanted ear. The ability to measure eSRT levels ipsilaterally can be improved by using a higher probe frequency.

Human middle-ear muscles rarely contract in anticipation of acoustic impulses: Implications for hearing risk assessments

The current study addressed the existence of an anticipatory middle-ear muscle contraction (MEMC) as a protective mechanism found in recent damage-risk criteria for impulse noise exposure. Specifically, the experiments reported here tested instances when an exposed individual was aware of and could anticipate the arrival of an acoustic impulse. In order to detect MEMCs in human subjects, a laser-Doppler vibrometer (LDV) was used to measure tympanic membrane (TM) motion in response to a probe tone. Here we directly measured the time course and relative magnitude changes of TM velocity in response to an acoustic reflex-eliciting (i.e. MEMC eliciting) impulse in 59 subjects with clinically assessable MEMCs. After verifying the presence of the MEMC, we used a classical conditioning paradigm pairing reflex-eliciting acoustic impulses (unconditioned stimulus, UCS) with various preceding stimuli (conditioned stimulus, CS). Changes in the time-course of the MEMC following conditioning were considered evidence of MEMC conditioning, and any indication of an MEMC prior to the onset of the acoustic elicitor was considered an anticipatory response. Nine subjects did not produce a MEMC measurable via LDV. For those subjects with an observable MEMC (n = 50), 48 subjects (96%) did not show evidence of an anticipatory response after conditioning, whereas only 2 subjects (4%) did. These findings reveal that MEMCs are not readily conditioned in most individuals, suggesting that anticipatory MEMCs are not prevalent within the general population. The prevalence of anticipatory MEMCs does not appear to be sufficient to justify inclusion as a protective mechanism in auditory injury risk assessments.

Human middle-ear muscles rarely contract in anticipation of acoustic impulses

The Auditory Hazard Assessment Algorithm for Humans (AHAAH) is an electrical equivalence model of the human ear designed to predict the risk for auditory injury from a given impulse noise exposure. One concern with the model is that the middle-ear muscle contraction (MEMC) associated with the acoustic reflex is implemented as a protective mechanism for certain instances in which a person is “warned” prior to the impulse. The current study tested the assumption that the MEMC can be elicited by a conditioning stimulus prior to sound exposure (i.e., a “warned” response). In order to quantify the MEMC, we used laser-Doppler vibrometry to measure tympanic membrane motion in response to a reflex-eliciting acoustic impulse. After verifying the MEMC, we attempted to classically condition the response by pairing the reflex-eliciting acoustic impulse (unconditioned stimulus, UCS) with various preceding stimuli (conditioned stimulus, CS). Changes in the magnitude and/or time-course of the MEMC following repeated UCS-CS pairings would be evidence of MEMC conditioning. Out of the 55 subjects tested so far, both non-conditioned (n = 53) and conditioned (n = 2) responses have been observed. These findings suggest that a “warned” MEMC may not be present in enough people to justify inclusion for being considered protective.

Anticipatory middle ear muscle contractions in damage-risk criteria

Anticipatory middle ear muscle contractions (MEMC) have been implemented as protective components of Damage-Risk Criteria (DRC) for impulsive noises. However, no studies have shown that anticipatory MEMC are pervasive among humans. This presentation describes a series of studies of the viability of assumed anticipatory MEMC obtained either through classical conditioning or while operating a model gun. Participants were adults with normal hearing, and the conditioning tasks varied on sensory modality and attention. Both between- and within-subjects designs were used. A conditioned response was defined as an MEMC occurring prior to the unconditioned stimulus and when only the conditioning stimulus was presented. These studies do not suggest that anticipatory MEMC should be included in DRC for impulsive noises.

Identifying the Origin of Effects of Contralateral Noise on Transient Evoked Otoacoustic Emissions in Unanesthetized Mice

Descending neural pathways in the mammalian auditory system are known to modulate the function of the peripheral auditory system. These pathways include the medial olivocochlear (MOC) efferent innervation to outer hair cells (OHCs) and the acoustic reflex pathways mediating middle ear muscle (MEM) contractions. Based on measurements in humans (Marks and Siegel, companion paper), we applied a sensitive method to attempt to differentiate MEM and MOC reflexes using contralateral acoustic stimulation in mice under different levels of anesthesia. Separation of these effects is based on the knowledge that OHC-generated transient evoked otoacoustic emissions (TEOAE) are delayed relative to the stimulus, and that the MOC reflex affects the emission through its innervation of OHC. In contrast, the MEM-mediated changes in middle ear reflectance alter both the stimulus (with a short delay) and the emission. Using this approach, time averages to transient stimuli were evaluated to determine if thresholds for a contralateral effect on the delayed emission, indicating potential MOC activation, could be observed in the absence of a change in the stimulus pressure. This outcome was not observed in the majority of cases. There were also no statistically significant differences between MEM and putative MOC thresholds, and variability was high for both thresholds regardless of anesthesia level. Since the two reflex pathways could not be differentiated on the basis of activation thresholds, it was concluded that the MEM reflex dominates changes in TEOAEs induced by contralateral noise. This result complicates the identification of purely MOC-induced changes on OAEs in mice unless the MEM reflex is inactivated surgically or pharmacologically.

Middle ear muscle contractions from non-acoustic elicitors

High-level sounds can elicit middle ear muscle contractions (MEMC), which are commonly known as acoustic reflexes. Tactile stimulation to the face can also elicit MEMC, and it is plausible that MEMC could co-occur with voluntary eye closure gestures. In this paper, we shall present preliminary MEMC results from human volunteers receiving controlled tactile stimulation (nitrogen gas, 10 kPa, 200 ms duration) to four locations on the face and who close the eye ipsilateral to the MEMC detection probe. The MEMC were detected via changes in total energy reflected in the ear using a filtered (0.2 to 8 kHz) click train. Concomitant muscle activity was measured using electromyography. The morphology and magnitude of the MEMC from these non-acoustic stimuli will be described. If non-acoustic MEMC behaviors do not extinguish and are not highly susceptible to fatigue, they could represent an opportunity to mediate exposure to short-duration noises or help explain between-person differences in noise exposure outcomes.

Assessment of the middle-ear assumption of the auditory hazard assessment algorithm for humans

The Auditory Hazard Assessment Algorithm for Humans (AHAAH) is an electrical equivalence model of the human ear designed to reproduce sound transmission from the outer into the inner ear in order to predict potential injury from a given sound exposure. This model was generated and validated using a (mostly) feline model, thus several key assumptions may not hold when adapted to the human. The current project aims to test some of these assumptions, such as the effects of middle-ear muscle contraction (MEMC) on sound transmission and whether the MEMC can be elicited by a conditioning stimulus prior to sound exposure (i.e., a “warned” response). In order to quantify the MEMC, we use laser-Doppler vibrometry to measure tympanic membrane motion in response to a reflex-eliciting acoustic impulse. After verifying the MEMC, we will attempt to classically condition the response by pairing the reflex-eliciting acoustic impulse (unconditioned stimulus, UCS) with a light from a LED display (conditioned stimulus, CS)....

On the origin of ear clicks during deglutition or pressure equalization

To explore the origin of clicking sounds in the ear during deglutition or other pharyngeal movements, which are interpreted differently in the literature. Experimental study at a tertiary referral centre. Acoustic phenomena during a forced opening test of the Eustachian tube (ET) were studied in a temporal bone model. Additionally, in vivo experiments were carried out in healthy volunteers for ruling out movements of the ossicular chain or the drumhead as potential causes of clicks. Thus, acoustic recordings were performed parallel to stapedius or tensor reflex measurements or pneumatic video endoscopies of the tympanic membrane. Obviously the acoustic signals (clicks) appear when the tube opens, which could be visualized and acoustically recorded during forced opening tests in temporal bone experiments. Middle ear muscle contractions with movements of the tympanic membrane did not cause any click events. Together with the results of a previous paper (9) we interpret the clicks as disruptions of fluid or mucus films covering the mucosa during the ET opening. The final goal of our studies is to use such clicks as indicators of ET openings in a new tube function test, which has to be elaborated.

Assessing acoustic reflexes for impulsive sound

The acoustic reflex is an involuntary contraction of the middle ear muscles in response to a variety of sensory and behavioral conditions. Middle ear muscle contractions (MEMC) have been invoked in some damage-risk criteria for impulsive noises for over 40 years and one damage-risk criteria proposes that MEMC precede the impulse for a warned listener via response conditioning. However, empirical data describing the prevalence, magnitude, and time-course of reflexive MEMC elicited by impulsive stimuli as well as non-acoustic stimuli and behaviors are scant. Likewise, empirical support for anticipatory MEMC is limited and studies often fail to control for attention or concomitant muscle activity. The current study is a large-scale, multi-experiment project designed to address these limitations in a laboratory and field environment. MEMC are detected using click train stimuli as probes. Reflexive MEMC are elicited using tones, recorded gunshots, and non-acoustic stimuli (e.g., controlled release of compresse...

Active control of ultrasonic hearing in frogs

Vertebrates can modulate the sound levels entering their inner ears in the face of intense external sound or during their own vocalizations. Middle ear muscle contractions restrain the motion of the middle ear ossicles, attenuating the transmission of low-frequency sound and thereby protecting the hair cells in the inner ear. Here we show that the Chinese concave-eared torrent frog, Odorrana tormota, can tune its ears dynamically by closing its normally open Eustachian tubes. Contrary to the belief that the middle ear in frogs permanently communicates with the mouth, O. tormota can close this connection by contraction of the submaxillary and petrohyoid muscles, drastically reducing the air volume behind the eardrums. Mathematical modeling and laser Doppler vibrometry revealed that the reduction of this air volume increases the middle ear impedance, resulting in an up to 20 dB gain in eardrum vibration at high frequencies (10-32 kHz) and 26 dB attenuation at low frequencies (3-10 kHz). Eustachian tube closure was observed in the field during calling and swallowing. Besides a potential role in protecting the inner ear from intense low-frequency sound and high buccal air pressure during calling, this previously unrecognized vertebrate mechanism may unmask the high-frequency calls of this species from the low-frequency stream noise which dominates the environment. This mechanism also protects the thin tympanic membranes from injury during swallowing of live arthropod prey.

Contralateral suppression of distortion product otoacoustic emissions and the middle-ear muscle reflex in human ears

Distortion product otoacoustic emissions (DPOAEs) were measured in the absence and presence of contralateral noise at five levels—below, equal to, and above the middle-ear muscle (MEM) reflex threshold. The resultant changes in DPOAE level and phase were dependent on stimulus frequency and noise level. Both low-level noise, believed to elicit the medial olivocochlear (MOC) reflex, and high-level noise, thought to activate both MOC and MEM reflexes, significantly decreased the DPOAE level. However, the shift from sole MOC effect to mixed MOC and MEM effects was not as dramatic as we thought. While low-level noise resulted in a minimum DPOAE phase change, high-level noise caused a substantial phase lead for 1 and 2 kHz. With increasing frequency, phase lag became more notable. The present study suggests the following: (1) DPOAE contralateral suppression by low-level sound most likely does not involve the effect of the MEM reflex and signal crossover; and (2) combined analysis of DPOAE level and phase changes warrants further investigations to overcome the difficulty in separating the effects of MOC efferents and MEM contraction. The results also imply that OAE measurement has the potential for being used to investigate the effect of the MEM reflex on sound transmission.

Hazard from impulse noise: Problems and prospects

Research findings continue to challenge the adequacy of existing impulse noise standards while consensus on a better formulation remains elusive. It is generally accepted that frequency weighting (reducing contribution of low frequencies) would be appropriate for impulse noise standards. However, data now present standards with twin problems which are opposite in character. On the one hand, the ear can be destroyed by intense exposures containing little energy (less than 10 J/m2) [Hamernik etal., J. Acoust. Soc. Am. 81, 1118–1129 (1987); Price and Wansack, J. Acoust. Soc. Am. 86, 2185–2191 (1989)]. Conversely, the ear can also tolerate immense amounts of energy at high intensities (≳100 kJ/m2) [Johnson and Paterson, Proc. 1992 Hearing Conserv. Conf. 103–106 (1992)]. A mathematical model of hearing hazard being developed [Price and Kalb, J. Acoust. Soc. Am. 90, 219–227 (1991)] promises to handle this complexity by incorporating a nonlinear stapes as well as middle ear muscle contractions into a hazard assessment, which is based on calculated basilar membrane displacements. Among other things, the model suggests that occasional exposure to intense impulses may be responsible for much of both occupational and nonoccupational noise-induced hearing loss.

Voluntary contraction of middle ear muscles: Effects on input impedance, energy reflectance and spontaneous otoacoustic emissions

Two types of measurements were performed on a subject able to voluntarily contract her middle ear muscles (MEM). First, wideband measurements (0–11 kHz) of middle ear input impedance and energy reflectance were obtained when the subject was relaxed and when she contracted her MEM. The changes in impedance observed with voluntary MEM contraction were similar to those reported in the literature for acoustically-elicited MEM contractions. The energy reflectance increased for frequencies below about 4 kHz. Second, the effects of voluntary MEM contraction on the frequencies and levels of spontaneous otoacoustic emissions (SOAEs) were measured and compared to effects evoked by contralateral acoustic stimulation. Effects on SOAEs appear to be a more sensitive indicator of MEM activity than changes in impedance, and the effects due to voluntary MEM contraction were qualitatively similar to those evoked by contralateral acoustic stimulation. These results suggest that in subjects with normally-functioning middle ears, only some effects on otoacoustic emissions caused by contralateral stimuli whose levels are below the contralateral acoustic reflex threshold can be unequivocally attributed to the action of cochlear efferents. The temporal aspects of SOAE frequency shifts caused by voluntary contraction of MEM show that voluntary contraction fatigues rapidly over a time period of tens of seconds.

Hypothetical roles of middle ear muscles in the guinea-pig

The attenuation of incoming sounds induced by acoustic reflex triggering was evaluated from the cochlear microphonic response to test tones in 45 awake guinea-pigs. Although control electromyographic measurements proved that the stapedius muscle was contracting, neither impedance changes nor attenuation induced by contralateral reflex-eliciting sounds were detectable in 30 cases out of 45. For ipsi- and bilateral stimulations, an attenuation was detectable for 7 guinea-pigs out of 10. In the guinea-pigs for which a reflex-induced change was found on CM, the mean attenuation was weak i.e. of the order of 2 dB at 20 dB above reflex threshold. These results were quite different from those obtained during control experiments in the rabbit for which CM attenuation was much larger. However, large attenuations associated with middle ear muscle contractions were found in the guinea-pig in other circumstances, i.e. during self-vocalization or when spontaneous muscle contractions occurred during anaesthesia. It is concluded that middle ear muscle can have several different functions, and that even when it exists, attenuation of loud sounds might not be their primary role.

Sonar gain control and echo detection thresholds in the echolocating bat, E p t e s i c u s f u s c u s

The echolocating bat, Eptesicus fuscus, detects sonar echoes with a sensitivity that changes according to the time elapsed between broadcasting of each sonar signal and reception of echoes. When tested in an electronic target simulator on a two-choice echo-detection task, the bat's threshold improved by 11.5 dB as echo delay changed from 2.3 to 4.6 ms (target ranges of 40 and 80 cm). Earlier experiments measured the change in detection threshold for delays from 1 to 6.4 ms (target ranges from about 17 to 110 cm) and obtained about 11 dB of improvement per doubling of delay. The new experiments used electronic delay lines to simulate echo delay, thus avoiding movement of loudspeakers to different distances and the possible creation of delay-dependent backward masking between stimulus echoes and cluttering echoes from the loudspeaker surfaces. The slope of the threshold shift defines an echo gain control that keeps echoes from point targets at a fixed sensation level--reducing sensitivity by 11 to 12 dB as echo amplitude increases by 12 dB per halving of range during the bat's approach to the target. A recent experiment using loudness discrimination of echoes at 70 to 80 dB SPL (roughly 50 dB above threshold) found a slope of about 6 dB per halving of range, so the gain-control effect may be level dependent. The observed effect is operationally equivalent to forward masking of echoes by the transmission, but any events correlated with vocalization which impair hearing sensitivity for a short interval following transmissions could cause a decline in sensitivity to echoes. Contractions of the bat's middle-ear muscles synchronized to transmissions may account for the observed threshold shift, at least for a span of echo delays associated with the most critical portion of the approach stage of pursuit. Forward masking by the sonar transmissions may contribute to the threshold shift, too, but middle-ear muscle contractions do occur and must be a significant part of the cause.