کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6277356 | 1295754 | 2010 | 8 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Differential activation of mitogen-activated protein kinases and brain-derived neurotrophic factor after temporary or permanent damage to a sensory system
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کلمات کلیدی
JnkTrkBPTSOHCERK 1/2ABRSPLTTSGAPDHPVDFBDNF - BDNF یا فاکتور نورونزایی مشتقشده از مغز MAPK - MAPKHearing loss - از دست دادن شنواییIHC - ایمونوهیستوشیمیRepair - تعمیرPermanent threshold shift - تغییر آستانه دائمیTemporary threshold shift - تغییر آستانه موقتProtection - حفاظتCochlea - حلزون گوشpolyvinylidene difluoride - دی فلوئورید پلی وینیلیدینSound pressure level - سطح فشار صوتOuter hair cells - سلول های موی بیرونیinner hair cells - سلول های موی درونیAuditory - شنواییBrain-derived neurotrophic factor - فاکتور نوروتروفی مشتق شده از مغزauditory brainstem response - پاسخ شنوایی مغزmitogen-activated protein kinases - کیناز پروتئین فعال Mitogenglyceraldehyde 3-phosphate dehydrogenase - گلیسرولیدید 3-فسفات دهیدروژنازNeurotrophin receptor - گیرنده نورورتیفین
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Functional and morphological differences between temporary (TTS) and permanent (PTS) hearing loss induced by acoustic trauma are well characterized whereas molecular differences remain to be elucidated. A comparative analysis of the expression of the phosphorylated forms of extracellular signal-regulated kinase (ERK1/2), c-jun-N-terminal kinases 1/2 (JNK1/2) and p38 in the mouse cochlea after acoustic trauma resulting in either a temporary or permanent damage is presented. In the acute phase of PTS an upregulation of phosphorylated p38, JNK1/2, and ERK1/2 was found while in the acute phase of TTS a downregulation of phospho-p38 occurred and no immediate change of pJNK1/2 and pERK1/2 was noted. After a 24 h recovery from TTS JNK1/2 and ERK1/2 was activated while the expression of phospho-p38 was downregulated. In contrast PTS group showed complete recovery to control values for all three MAPKs by 24 h post. The level of brain-derived neurotrophic factor (BDNF), a potent otoprotective agent, was elevated after both types of acoustic trauma but the elevation after permanent trauma was of a longer duration. The expression of BDNF receptor's TrkB (truncated form) was downregulated only after permanent hearing loss. Thus, temporary and permanent hearing loss demonstrate different expression patterns and temporal aspects of MAPK, BDNF and TrkB in the cochlea. The results of this study will help reveal the cellular mechanisms underlying hearing loss induced by acoustic trauma.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 165, Issue 4, 17 February 2010, Pages 1439-1446
Journal: Neuroscience - Volume 165, Issue 4, 17 February 2010, Pages 1439-1446
نویسندگان
I. Meltser, Y. Tahera, B. Canlon,