کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6286399 | 1615305 | 2013 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Long-lasting changes in the cochlear K+ recycling structures after acute energy failure
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کلمات کلیدی
PBSABR3NPNKCC1Kir4.1Cx263-nitropropionic acid - 3-اسید نیتروپروپیونیکL-PGDS - PGDSMitochondrial dysfunction - اختلال در عملکرد میتوکندریHearing loss - از دست دادن شنواییSudden sensorineural hearing loss - افت شنوایی ناگهانی حسی عصبیRecovery - ریکاوریStria vascularis - عروق کرونرPhosphate buffered saline - فسفات بافر شورlipocalin-type prostaglandin D synthase - لیپوکالین پروستاگلاندین D سنتازauditory brainstem response - پاسخ شنوایی مغزConnexin 26 - کانکسین 26
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Fibrocytes in the cochlear lateral wall and spiral limbus play an important role in transporting K+ and have the capacity of self-renewal. We showed that acute energy failure in the rat cochlea induced by local administration of the mitochondrial toxin 3-nitropropionic acid (3NP) caused hearing loss in a concentration-dependent manner, mainly due to degeneration of cochlear fibrocytes. We produced long-lasting profound cochlear damage in this model by modifying the 3NP administration protocol and observed morphological changes at 16 weeks after the administration. In the spiral ligament, severe degeneration of fibrocytes was observed in the basal turn, and the levels of the Na,K-ATPase alpha and beta1 subunits and of NKCC1 were decreased in these cells, whereas connexin 26 (Cx26) level increased in the type 1 fibrocytes adjacent to the stria vascularis. In the stria vascularis, levels of Kir4.1 and L-PGDS decreased. In the spiral limbus, severe degeneration of fibrocytes was observed in the middle and basal turns, but NKCC1 and Cx26 were still found in the center of the limbus in the middle turn. These results indicate long-lasting changes in the cochlear lateral wall and spiral limbus, which may compensate for damaged K+ recycling and protect cells from ATP shortage.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience Research - Volume 77, Issues 1â2, SeptemberâOctober 2013, Pages 33-41
Journal: Neuroscience Research - Volume 77, Issues 1â2, SeptemberâOctober 2013, Pages 33-41
نویسندگان
Yoichiro Takiguchi, Guang-wei Sun, Kaoru Ogawa, Tatsuo Matsunaga,