{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,20]],"date-time":"2025-10-20T16:23:40Z","timestamp":1760977420423},"reference-count":38,"publisher":"Acoustical Society of America (ASA)","issue":"2","content-domain":{"domain":["pubs.aip.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[1998,8,1]]},"abstract":"<jats:p>The suppression tuning of distortion-product otoacoustic emissions (DPOAEs) is commonly assumed to measure frequency selectivity, because the dominant features of suppression-tuning curves (STCs) are similar to the principal properties of the neural-tuning curves (NTCs) of single auditory-nerve fibers. In the present study, several common loop diuretics were used to affect the DPOAE-generation process to determine if reversible ototoxicity could adversely modify the characteristics of STCs, in a manner similar to that shown previously for NTCs. Contour plots of DPOAE level in the presence of a series of variable-level suppressor tones were obtained before and after administering diuretic drugs that reversibly reduced or eliminated DPOAEs. Primary-tone pairs were centered at 2.8 or 4 kHz, with L1=L2, or L2&amp;lt;L1. From the resulting plots, STC parameters including tip frequency, threshold at the tip frequency, and Q10\u2009dB measures of tuning were extracted for four suppression criteria of 3, 6, 9, and 12 dB. In the pre-drug nonototoxic state, suppression tuning depended on both primary-tone level (L1,L2), and the relative levels of the primaries (L1\u2212L2), with tuning being sharper for lower- than for higher-level equilevel primaries, and sharpest for offset-level primary tones. Following drug injection, the expected decrease in sharpness of tuning evidenced by changes in Q10\u2009dB as well as the dramatically elevated tip thresholds normally seen for NTCs under similar conditions, were not observed. Overall, Q10\u2009dB increased or decreased more or less randomly, with a slight tendency for STCs to become sharper than prior to drug dosing, for the two highest suppression criteria. The STC-tip frequencies demonstrated significant decreases following diuretic administration that were weakly correlated with the associated decreases in DPOAE amplitude. The most consistent changes in response to the drug-induced reduction in DPOAE level were increases in the STC-tip thresholds. However, these changes were relatively small and rarely exceeded 10 dB. In the absence of notable changes in overall STC shape, a major finding was a change in the effectiveness of suppression following ototoxic insult. However, when the amount of suppression was expressed as a percentage of the DPOAE remaining, the effects of diuretic dosing were often almost completely obscured. Overall, the results demonstrated that when the generation of DPOAEs was interfered with by the introduction of a suppressor tone to produce STCs that resemble NTCs, STCs behaved quite differently following reversible cochlear insult than their previously documented neural counterparts. These findings imply that STCs do not assess the frequency-selective aspects of the cochlear amplification process in a manner similar to NTCs.<\/jats:p>","DOI":"10.1121\/1.423340","type":"journal-article","created":{"date-parts":[[2002,7,26]],"date-time":"2002-07-26T14:05:41Z","timestamp":1027692341000},"page":"972-983","update-policy":"http:\/\/dx.doi.org\/10.1063\/aip-crossmark-policy-page","source":"Crossref","is-referenced-by-count":35,"title":["Effects of loop diuretics on the suppression tuning of distortion-product otoacoustic emissions in rabbits"],"prefix":"10.1121","volume":"104","author":[{"given":"Glen K.","family":"Martin","sequence":"first","affiliation":[{"name":"Department of Otolaryngology, University of Miami School of Medicine, P.O. Box 016960, Miami, Florida 33101-6960"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"David","family":"Jassir","sequence":"additional","affiliation":[{"name":"Department of Otolaryngology, University of Miami School of Medicine, P.O. Box 016960, Miami, Florida 33101-6960"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Barden B.","family":"Stagner","sequence":"additional","affiliation":[{"name":"Department of Otolaryngology, University of Miami School of Medicine, P.O. Box 016960, Miami, Florida 33101-6960"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Brenda L.","family":"Lonsbury-Martin","sequence":"additional","affiliation":[{"name":"Department of Otolaryngology, University of Miami School of Medicine, P.O. 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