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Ischemia was induced by bilaterally occluding the vertebral arteries for 5 minutes in gerbils, which lack posterior cerebral communicating arteries. In gerbils, the labyrinthine arteries are fed solely by the vertebral arteries. Occlusion of the vertebral arteries caused a remarkable increase in the threshold of compound action potentials (CAPs), which recovered over the following day. However, 7 days after the onset of reperfusion, the threshold began to increase again. Morphologic changes in the hair cell stereocilia were revealed by electron microscopy. The number of nuclear collapses was counted in cells stained for DNA and F\u2010actin to evaluate the degree of cell death in the organ of Corti. Changes in spiral ganglion cell (SGC) neuron number were detected, whether or not progressive neuronal death occurred in the SGC. These studies showed that sporadic fusion of hair cells and the disappearance of hair cell stereocilia did not begin until 4 days after ischemia. On subsequent days, the loss of hair cells, especially inner hair cells (IHCs), and the degeneration of SGC neurons became apparent. Ten days after ischemia, the mean percentage cell loss of IHCs was 6.4% in the basal turn, 6.4% in the second turn, and 0.8% in the apical turn, respectively, and the number of SGC neurons had decreased to 89% of preischemic status. These results indicate that transient ischemia causes delayed hearing loss and cell death in the cochlea by day 7 after ischemia. J. Comp. Neurol. 456:105\u2013111, 2003. \u00a9 2002 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/cne.10479","type":"journal-article","created":{"date-parts":[[2003,1,15]],"date-time":"2003-01-15T21:02:30Z","timestamp":1042664550000},"page":"105-111","source":"Crossref","is-referenced-by-count":38,"title":["Transient cochlear ischemia causes delayed cell death in the organ of Corti: An experimental study in gerbils"],"prefix":"10.1002","volume":"456","author":[{"given":"Kenichiro","family":"Koga","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nobuhiro","family":"Hakuba","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Futoshi","family":"Watanabe","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Masachika","family":"Shudou","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Takayuki","family":"Nakagawa","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kiyofumi","family":"Gyo","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2002,12,31]]},"reference":[{"key":"e_1_2_5_2_1","doi-asserted-by":"publisher","DOI":"10.1002\/ar.1090940210"},{"key":"e_1_2_5_3_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1471-4159.1984.tb05396.x"},{"key":"e_1_2_5_4_1","doi-asserted-by":"publisher","DOI":"10.1007\/BF00453725"},{"key":"e_1_2_5_5_1","doi-asserted-by":"publisher","DOI":"10.1016\/0378-5955(89)90010-5"},{"key":"e_1_2_5_6_1","doi-asserted-by":"publisher","DOI":"10.1016\/0378-5955(93)90125-K"},{"key":"e_1_2_5_7_1","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1993.73.2.309"},{"key":"e_1_2_5_8_1","doi-asserted-by":"publisher","DOI":"10.1016\/0378-5955(87)90024-4"},{"key":"e_1_2_5_9_1","doi-asserted-by":"crossref","first-page":"329","DOI":"10.1007\/BF00453558","article-title":"Occlusion of inner ear vessels by magnetic forces applied to circulating metallic iron particles","volume":"242","author":"Giebel W","year":"1985","journal-title":"Arch Otorhinolaryngol"},{"key":"e_1_2_5_10_1","doi-asserted-by":"crossref","first-page":"313","DOI":"10.5631\/jibirin.91.313","article-title":"Ischemia\u2010induced hearing loss and glutamate efflux in the perilymph; 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