TY - JOUR
T1 - Late-phase recovery in the cochlear lateral wall following severe degeneration by acute energy failure
AU - Mizutari, Kunio
AU - Nakagawa, Susumu
AU - Mutai, Hideki
AU - Fujii, Masato
AU - Ogawa, Kaoru
AU - Matsunaga, Tatsuo
N1 - Funding Information:
Grant information: This study was supported by a Health Science Research Grant ( H16-kankakuki-006 ) from the Ministry of Health, Labour and Welfare of Japan (T.M.), and a Grant-in-Aid for Young Scientists (B) ( 18791251 to K.M.) from the Ministry of Education, Culture, Sports, Science and Technology of Japan .
PY - 2011/10/24
Y1 - 2011/10/24
N2 - We previously reported a model of acute cochlear energy failure using a mitochondrial toxin, 3-nitropropionic acid (3-NP), to study mechanisms of inner ear disorders such as inner ear ischemia. In this model, the main cause of hearing loss is apoptosis of fibrocytes in the cochlear lateral wall. Here, we analyzed the time course of structural and hearing level changes in the cochlea from the acute phase to the chronic phase up to 2 months after surgery. Hearing levels as determined by auditory brainstem response (ABR) thresholds exceeded the maximum acoustic output (> 87 dBSPL) of the system at all frequencies 1 day after 3-NP treatment. Histology showed nearly complete loss of fibrocytes 2 weeks after 3-NP treatment. However, after 2 months, ABR showed significant recovery at low frequency (8 kHz) in four of five rats treated with 3-NP. ABR thresholds at 20 kHz occasionally showed some recovery. At 40 kHz, recovery of ABR thresholds was not observed. Histology of 3-NP-treated rats revealed partial recovery of the lateral wall and the regenerated fibrocytes in the spiral ligament expressed Na/K-ATPase in the cochlear basal turn 2 months after 3-NP treatment. These results indicate that ABR recovery is caused by regeneration of the cochlear lateral wall. Our findings demonstrate the recoverable capacity of the cochlear lateral wall that leads to functional recovery after severe damage.
AB - We previously reported a model of acute cochlear energy failure using a mitochondrial toxin, 3-nitropropionic acid (3-NP), to study mechanisms of inner ear disorders such as inner ear ischemia. In this model, the main cause of hearing loss is apoptosis of fibrocytes in the cochlear lateral wall. Here, we analyzed the time course of structural and hearing level changes in the cochlea from the acute phase to the chronic phase up to 2 months after surgery. Hearing levels as determined by auditory brainstem response (ABR) thresholds exceeded the maximum acoustic output (> 87 dBSPL) of the system at all frequencies 1 day after 3-NP treatment. Histology showed nearly complete loss of fibrocytes 2 weeks after 3-NP treatment. However, after 2 months, ABR showed significant recovery at low frequency (8 kHz) in four of five rats treated with 3-NP. ABR thresholds at 20 kHz occasionally showed some recovery. At 40 kHz, recovery of ABR thresholds was not observed. Histology of 3-NP-treated rats revealed partial recovery of the lateral wall and the regenerated fibrocytes in the spiral ligament expressed Na/K-ATPase in the cochlear basal turn 2 months after 3-NP treatment. These results indicate that ABR recovery is caused by regeneration of the cochlear lateral wall. Our findings demonstrate the recoverable capacity of the cochlear lateral wall that leads to functional recovery after severe damage.
KW - 3-nitropropionic acid (3-NP)
KW - Cochlear lateral wall
KW - Fibrocyte
KW - Recovery
KW - Spiral ganglion
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U2 - 10.1016/j.brainres.2011.08.062
DO - 10.1016/j.brainres.2011.08.062
M3 - Article
C2 - 21925650
AN - SCOPUS:80054095561
SN - 0006-8993
VL - 1419
SP - 1
EP - 11
JO - Brain Research
JF - Brain Research
ER -