{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,16]],"date-time":"2025-10-16T13:49:32Z","timestamp":1760622572119},"reference-count":34,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2007,8,24]],"date-time":"2007-08-24T00:00:00Z","timestamp":1187913600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J of Neuroscience Research"],"published-print":{"date-parts":[[2008,1]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>We recently showed that acute energy failure in the rat cochlea induced by local administration of the mitochondrial toxin 3\u2010nitropropionic acid (3\u2010NP) causes hearing loss mainly due to degeneration of cochlear lateral\u2010wall fibrocytes. In the present study, we analyzed the effect of the pan\u2010caspase inhibitor z\u2010Val\u2010Ala\u2010Asp(Ome)\u2010fluoromethylketone (Z\u2010VAD\u2010FMK) on 3\u2010NP\u2010induced hearing loss in a model showing temporary threshold shifts at low frequencies and permanent threshold shifts at high frequencies. The model rats received an intraperitoneal injection of either Z\u2010VAD\u2010FMK or vehicle for 3 days starting 1 day prior to 3\u2010NP treatment. One day after the administration of 3\u2010NP, the auditory brain\u2010stem response (ABR) threshold at 20 kHz was elevated to 70 dB in the Z\u2010VAD\u2010FMK group and to 85 dB in controls. The Z\u2010VAD\u2010FMK group completely recovered to the preoperative level within 14 days, whereas in the controls, the ABR threshold remained elevated at 50 dB even 28 days after the administration of 3\u2010NP. Treatment with Z\u2010VAD\u2010FMK also improved recovery of hearing at 8 kHz but did not change recovery at 40 kHz. Histological examination demonstrated that treatment with Z\u2010VAD\u2010FMK inhibited progressive degeneration of the lateral\u2010wall fibrocytes in the cochlear basal turn, as well as apoptosis of these fibrocytes. These results clearly indicate that caspase\u2010dependent apoptosis of fibrocytes in the cochlear lateral wall plays an important role in hearing loss in the present animal model. Moreover, the results of the present study suggest that systemic administration of a caspase inhibitor may be an effective therapy for sensorineural hearing loss caused by acute energy failure such as that observed in cochlear ischemia. \u00a9 2007 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/jnr.21470","type":"journal-article","created":{"date-parts":[[2007,8,25]],"date-time":"2007-08-25T01:54:50Z","timestamp":1188006890000},"page":"215-222","source":"Crossref","is-referenced-by-count":23,"title":["Caspase inhibitor facilitates recovery of hearing by protecting the cochlear lateral wall from acute cochlear mitochondrial 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