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Nov 1979

Volume 66, Issue S1, pp. S1-S89

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back to top Session X. Physiological Acoustics III: Cochlea, Auditory Nerve, and Models (Poster Session)
Contributed Papers
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The role of potassium and sodium in cochlear transduction: A study with amiloride and tetraethylammonium (A)

A. N. Salt and T. Konishi

J. Acoust. Soc. Am. Volume 66, Issue S1, pp. S47-S47 (1979); (1 page)

Online Publication Date: 11 Aug 2005

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The effects of amiloride and tetraethylammonium (TEA) on cochlear microphonics (CM), action potentials (AP), and endocochlear potential (EP) were studied in guinea pigs. It has been reported that amiloride selectively reduces sodium permeability in a variety of ion transporting epithelia. Perilymphatic perfusion (10−3 M) or intravenous administration (20 mg/kg) of amiloride suppressed AP, but did not significantly alter CM or EP. Application of amiloride to the endolymph by iontophoretic or perfusion techniques also produced no greater changes of CM and EP than were observed during control procedures. TEA has been shown to suppress the potassium permeability increase in excitable cell membranes. Perilymphatic perfusion of TEA (10‐2 M) did not suppress CM or EP, but AP was reduced. Iontophoretic application of TEA to the endolymph markedly suppressed CM, while EP increased in value. The effects of TEA applied to the endolymph were similar to those effects previously reported to occur during noise exposure (J. Acoust. Soc. Am. Suppl. 1 64, S132(A) (1978)]. This result adds support to the hypothesis that noise induced CM suppression is a consequence of a potassium permeability decrease of the endolymph/perilymph barrier. The contribution of sodium ion movements to cochlear transduction appears less certain in the light of the insensitivity of CM and EP to amiloride.
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Maintenance of cochlear function with synthetic blood and effects of potassium deficiency (A)

R. Thalmann, J. Kambayashi, J. Wada, J. E. DeMott, and D. Marcus

J. Acoust. Soc. Am. Volume 66, Issue S1, pp. S47-S47 (1979); (1 page)

Online Publication Date: 11 Aug 2005

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We have recently described a method for the vascular perfusion of the guinea pig cochlea with synthetic blood, using the flurocarbon FC 47 as oxygen carrier [Wada et al., Laryngoscope (1979) (to be published)]. We have now determined that the endolymphatic potential (EP) and the cochlear microphonics can be maintained at normal or near normal levels for perfusion periods exceeding 300 and 150 min, respectively. However, the compound action potential (N1) cannot be maintained for longer than 60 min. This finding may be of considerable significance for blood substitute technology in general, since N1 could be the most sensitive indicator of adverse effects of synthetic blood known to date. In other experiments we found that the EP can be maintained at normal levels for 25.3 ± 6.9 (SD) minutes by K+‐free vascular perfusion. By contrast, the EP starts to decline immediately if perilymph is replaced by K+‐free media [Marcus et al., J. Acoust. Soc. Am. Suppl. 1 65, S13(A) (1979)]. The possible implications of these findings with regard to the mode of generation of the EP will be discussed. [Supported by the NIH and NSF.]
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Effects of substrate free vascular perfusion of the cochlea (A)

J. Kambayashi, J. E. DeMott, T. H. Comegys, I. Thalmann, N. Y. Marcus, and R. Thalmann

J. Acoust. Soc. Am. Volume 66, Issue S1, pp. S47-S47 (1979); (1 page)

Online Publication Date: 11 Aug 2005

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During vascular perfusion of the cochlea with substrate free synthetic blood, the endolymphatic potential (EP) is maintained for 85 ± 20 (SD) minutes. The subsequent decline of the EP can be prevented by 0.8 mM glucose or by 11 mM lactate, but not by succinate (although 20 mM succinate effects a partial recovery of the EP when it has declined by 40 mV). Significant breakdown of strial glycogen occurs only when the EP starts to decline. Glycogen stores in the stria are virtually depleted when the EP has dropped to about 30 mV. At about the same time, the further decline of the EP is arrested, presumably due to activation of a new substrate pool. Only following a stabilization of some 30 min does the EP resume its decline. It appears that the prolonged initial maintenance of the EP during substrate free vascular perfusion is due to the utilization of glucose from cochlear fluids, since the EP starts to decline immediately when the perilymphatic glucose pool is removed simultaneously by perilymphatic perfusion. [Supported by NIH and NSF.]
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Levels of putative neurotransmitters, glutamate and aspartate, in cochlear fluids and cell layers of organ of Corti (A)

I. Thalmann, R. Thalmann, D. C. Marcus, and T. H. Comegys

J. Acoust. Soc. Am. Volume 66, Issue S1, pp. S47-S47 (1979); (1 page)

Online Publication Date: 11 Aug 2005

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Glutamate and/or aspartate have been proposed as transmitters in acoustico‐lateralis systems. We analyzed these substances in cochlear fluids of guinea pigs and in cell layers of organ of Corti of chinchillas. Fluids were collected with utmost care to avoid contamination. Concentrations of aspartate were 2.6 ± 1.2 (SD) and 16.3 ± 3.5 μM in perilymph and endolymph, respectively. Corresponding values for glutamate were 11.9 ± 5.0 and 74.0 ± 6.5 μM. Aspartate exhibited a gradient in whole organ of Corti [52 units (mmoles/kg dry weight) in third versus 109 units in basal turn]. No specific accumulations were seen in inner or outer hair cell layers; in fact, concentrations were highest in Hensen and Claudius cells. Glutamate exhibited only a slight gradient in organ of Corti (60 units in basal versus 81 units in third turn). Levels were similar in outer hair cell layer and supporting cells, but significantly lower in inner hair cell layer. No definite conclusions about a possible transmitter role of either substance can be drawn from these data. [Supported by NIH and NSF.]
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Stimulus‐induced release of endogenous amino acids from the Xenopus laevis lateral‐line organ (A)

S. C. Bledsoe, Jr., R. P. Bobbin, R. Thalmann, and I. Thalmann

J. Acoust. Soc. Am. Volume 66, Issue S1, pp. S47-S48 (1979); (2 pages)

Online Publication Date: 11 Aug 2005

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Previously, we described a method for studying stimulus‐induced release of substances from the Xenopus lateral line [Bledsoe et al., J. Acoust. Soc. Am. Suppl. 1 65, S11(A) (1979)]. To date, 13 experiments have been completed in which the release of endogenous amino acids was studied by comparing the effects of pulsatile water motion on the efflux of glutamate and aspartate from isolated skins with and without lateral‐line stitches. For a given experiment paired stitch and nonstitch skins were subjected to two. 30‐min periods of stimulation and two, 30‐min periods of no stimulation in a rotated order‐of‐occurrence. In an overall comparison of mean amino acid levels for the first and second periods of the stimulated versus nonstimulated conditions, stimulation applied to the outer skin surface caused a significant increase in glutamate and aspartate efflux from stitch (p < 0.01) and nonstitch (p < 0.01) skins. The stimulated efflux of glutamate from stitch skins was significantly greater than the stimulated efflux from nonstitch skins (p < 0.01). For aspartate efflux the between skin comparison was less clear cut with stimulation causing a significantly greater efflux from stitch skins than from nonstitch skins (p < 0.01), only when comparing the mean aspartate levels for the first periods of the stimulated versus nonstimulated conditions. Although the source and mechanisms underlying the greater stimulated efflux from stitch skins remain to be determined, the results demonstrate differences between stitch and nonstitch skins under stimulus conditions which should induce release of the afferent transmitter substance(s). [Work supported by NIH and The Kresge Foundation.]
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Effects of acute noise traumata on cochlear frequency analysis as observed in whole‐nerve and single‐cell recordings (A)

E. van Heusden and G. F. Smoorenburg

J. Acoust. Soc. Am. Volume 66, Issue S1, pp. S48-S48 (1979); (1 page)

Online Publication Date: 11 Aug 2005

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Tuning curves were obtained in cat by masking the whole‐nerve action potential (AP), applying a forward‐masking paradigm. The Q10 values of the tuning curves appeared to be about half the values found for threshold tuning curves of single nerve fibers. After inducement of a noise trauma by a 105 dB SPL wide‐band noise that lasted for 30 min, Q10 values of the AP tuning curves became noticeably smaller. We carefully checked that this decrease of Q10 should be attributed to a loss in tuning selectivity and not to changes in the masking phenomenon itself. A decrease of Q10 values due to the noise trauma was found also for tuning of single cells in the anteroventral cochlear nucleus. For both the whole‐nerve and the single‐cell responses, the decrease of Q10 is not simply an effect of stimulus level. The decrease is found for tuning curves just above pre‐ and post‐trauma thresholds as well as for tuning curves at the same SPL before and after inducement of the trauma. [Research supported by the Netherlands Organization for the Advancement of Pure Research, ZWO.]
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The acoustical inverse problem for the cochlea (A)

Man Mohan Sondhi

J. Acoust. Soc. Am. Volume 66, Issue S1, pp. S48-S48 (1979); (1 page)

Online Publication Date: 11 Aug 2005

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A knowledge of the spatially varying mechanical properties of the basilar membrane (BM) allows one to compute acoustical properties of the cochlea, e.g., the transfer function from stapes to a point on the BM. However, to the best of our knowledge, direct measurements of BM properties have not been reported in the literature. Rather, these properties are “estimated” by trial and error so as to give a reasonable match to measurements of the above‐mentioned transfer function. In this talk we will show how the BM stiffness K(x) may be determined directly from a time‐domain measurement of the input impedance at the stapes (i.e., from a measurement of the pressure developed just inside the stapes in response to an impulse of stapes velocity).
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A mode of peripheral auditory processing (A)

R. A. Houde, J. C. Bancroft, and C. W. Parkins

J. Acoust. Soc. Am. Volume 66, Issue S1, pp. S48-S48 (1979); (1 page)

Online Publication Date: 11 Aug 2005

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A model of peripheral auditory processing was developed to guide the experimental design of a multichannel cochlear implant. The model specifies the neural processing necessary to represent observed PST histogram behavior of single eighth‐nerve neurons and its relationship to the design of a multichannel vocoder processor. The model includes electrical characteristics of the cochlea. Simulation studies of stimulation characteristics are reported.
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Modulation of cochlear nerve fiber activity by low frequencies (A)

K. Ingvarsson and P. Dallos

J. Acoust. Soc. Am. Volume 66, Issue S1, pp. S48-S48 (1979); (1 page)

Online Publication Date: 11 Aug 2005

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A 100‐Hz tone of relatively high intensity (40–80 dB SPL) has a modulating effect on the activity of auditory fibers when the cochlea is stimulated with this tone and a tone at the characteristic frequency (CF). This effect can be noted even when the low‐frequency tone itself does not stimulate the fiber. The phase of the 100‐Hz tone at which enhancement of activity driven by the CF‐tone is seen to occur corresponds to the phase where the 100‐Hz tone alone elicits activity. In fibers of CF greater than 2 kHz, the velocity component of the 100‐Hz tone is not appreciable, compared to the CF velocity component. Thus the effect described lends support to the theory that the static position of the basilar membrane has a biasing effect on the inner hair cell excitation. [Supported by grants from the NINCDS.]
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Two‐tone suppression in the auditory nerve of the cat: Suppression thresholds and rate of growth (A)

Eric Javel

J. Acoust. Soc. Am. Volume 66, Issue S1, pp. S48-S48 (1979); (1 page)

Online Publication Date: 11 Aug 2005

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Our previous work has been directed at elucidating the behavior of the two‐tone suppression phenomena when both tones are excitatory. Analyzing the phase‐locked response of fibers possessing low characteristic frequency (CF), we have shown [E. Javel, J. Acoust. Soc. Am. Suppl. 1 65, S83(A) (1979)] that suppression exists throughout an auditory nerve fiber's response area and that the ability of an excitatory tone to suppress the response to another excitatory tone is similar to a nonexcitatory tone's ability to suppress. For a given suppressor‐tone intensity, suppression is maximal when the suppressor tone lies near fiber CF, and suppression magnitude is reduced on either side of CF. The contours relating suppression magnitude to frequency are similar in shape, but not in extent, to the isointensity response contours observed in determinations of response area. The “threshold” for suppression is systematically related to fiber sensitivity at the suppressor‐tone frequency, but it is always greater or equal to the pure‐tone threshold at that frequency. Threshold for suppression is not related to the threshold for the tone being suppressed. Once the threshold is exceeded, suppression for both excitatory and nonexcitatory tones grows with increasing suppressor‐tone intensity in a manner consistent with that described by Sachs and Abbas [J. Acoust. Soc. Am. 60, 1157–1163 (1976)]. The final slope of the curve relating suppression magnitude to suppressor‐tone intensity is near unity for suppressor frequencies near fiber CF, but is usually greater than one for suppressors much lower in frequency than CF and less than one for suppressors higher in frequency than CF. Suppression does not saturate at high intensities, but in many instances its magnitude is obscurred by the “notch” often seen in single‐tone rate‐intensity functions [Kiang et al., J. Acoust. Soc. Am. 46, 106(A) (1969)], i.e., the “notch” cannot be suppressed. [Work supported by NIH.]
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AP responses in forward‐masking paradigms and their relationship to responses of auditory‐nerve fibers (A)

Paul J. Abbas and Michael P. Gorga

J. Acoust. Soc. Am. Volume 66, Issue S1, pp. S48-S49 (1979); (2 pages)

Online Publication Date: 11 Aug 2005

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The amplitude of N, peaks of whole‐nerve AP was measured in cats using a tone‐burst probe with tonal maskers in a forward‐masking paradigm. Experiments examined the effects of masker level, frequency, and duration (Tm), as well as interstimulus interval (Δt). Results are consistent with the interpretation that amplitude of N1 reflects activity of a limited group of fibers with CF near the probe frequency. For single fibers, decrement in discharge rate (relative to an unmasked condition) is dependent upon rate to the masker [Smith, J. Neurophysiol. 40, 1088–1112 (1977)]. For the AP, decrement in probe‐elicited amplitude should reflect the rate to the masker in those fibers excited by the probe. Thus, measurements of N1 decrement versus masker frequency and level are similar to single‐fiber rate‐versus‐level functions. Since decrement in N1 reflects amount of adaptation, increasing Tm decreases probe response. N1 amplitude as a function of Tm thus resembles PST histograms of nerve fibers. Finally, plots of N1 amplitude as a function of Δt are interpreted as a measure of recovery from adaptation.
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AP tuning curves and anatomical correlates from acoustically traumatized cats (A)

N. T. Shepard and P. J. Abbas

J. Acoust. Soc. Am. Volume 66, Issue S1, pp. S49-S49 (1979); (1 page)

Online Publication Date: 11 Aug 2005

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Compound action potential tuning curves, using a forward‐masking paradigm, were developed on both a control group and a group of acoustically traumatized cats. Differences observed between the two populations included a decrease in the sharpness of the tip, in the sensitivity of the tip, and/or in the sensitivity of the tail region. Phase contrast light microscopy was performed on all exposed ears using a celloidin embedding technique with horizontal sectioning. Whenever an abnormality in an AP tuning curve was seen, histological evidence of damage to the organ of Corti in an appropriate region corresponding to the signal frequency was observed. However, several cases of damage to the cochlea were observed with normal tuning curves. Wherever the tip region of the tuning curve was elevated, evidence of damage to all three rows of OHC and to the IHC was seen. Several other observations relating to the extent of damage to the OHC and IHC independently were found to be similar to results from single‐fiber recordings in acoustically traumatized cats [M. C. Liberman and N. Y. Kiang, Acta Otolaryngol. Suppl (STOCKH) (358). 1–63 (1978)].
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High‐frequency sensitivity of the frog basilar papilla confirmed by dye injection (A)

E. L. Leverenz and E. R. Lewis

J. Acoust. Soc. Am. Volume 66, Issue S1, pp. S49-S49 (1979); (1 page)

Online Publication Date: 11 Aug 2005

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High‐frequency sensitivity (cf. in the range 1000 to 2000 Hz) has been confirmed in the basilar papilla of the bullfrog by recording the responses of single eighth‐nerve axons, then injecting those axons with the fluorescent dye Lucifer Yellow, and thereby tracing them to their origins at the periphery. Dye‐filled glass micropipettes were used to penetrate primary afferent axons in the posterior branch of the eighth cranial nerve medial to its emergence from the intact otic capsule with intact circulation. All axons that we have traced to the basilar papilla have been of the high‐frequency type [Feng et al., J. Comp. Physiol. 100, 221–229 (1975)], while all units that we have traced to the amphibian papilla have been of the low‐ or mid‐frequency type. So far, all primary afferent axons traced to the basilar papilla have been unbranched and have innervated one or perhaps two hair cells. Our direct observations of high‐frequency sensitive fibers emanating from the basilar papilla confirm the conclusions drawn previously by Frishkopf, Capranica, and Goldstein [Proc. IEEE 56, 969–980 (1968)]; Fend et al. (op. cit.); and others.
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Some new causes of acoustic impedance change during acoustic stimulation in man (A)

V. R. Singh

J. Acoust. Soc. Am. Volume 66, Issue S1, pp. S49-S49 (1979); (1 page)

Online Publication Date: 11 Aug 2005

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Investigation of the actual nature and causes of the acoustic impedance change during acoustic stimulation in the ear has been an active area in the recent past. It is believed that the impedance change is only due to the middle ear muscle activity, but according to the present investigation, this is not true. The acoustic impedance has been studied with and without ipsilateral sound stimulus by using an electroacoustic bridge technique in living human ears, temporal bones, and mechanical models of the ear. The change in the acoustic impedance is also found in denerved cadaver bones and mechanical ears. This clearly shows that the muscle activity is not the only cause, but some new causes like physiological characteristics of the eardrum, anatomical structures of the ear, local induction phenomenon in the ear, and compliance of the eustachian tube are also responsible for the acoustic impedance change during the sound stimulation. The present study is useful in investigating the actual nature and causes of infections and diseases of the ear. [Work supported by Canadian Commonwealth Scholarship and Fellowship Committee.]
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