کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6278751 | 1295856 | 2006 | 12 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Regulation of cocaine-induced activator protein 1 transcription factors by the extracellular signal-regulated kinase pathway
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کلمات کلیدی
CREBNacbTBSERKPFASREIEGAP-1MAPK - MAPKelectromobility shift assay - آزمایش الکتریکی حرکتیStriatum - استریاتومAddiction - اعتیاد Gene expression - بیان ژنTris-buffered saline - تریس بافر شورDopamine - دوپامینEMSA یا electrophoretic mobility shift assay - سنجش تغییر تحرک الکتروفورتیکSerum response element - عنصر پاسخ سرمNucleus accumbens - هسته accumbensCaudate putamen - پاتامن Caudateparaformaldehyde - پارافرمالدهیدactivator protein 1 - پروتئین فعال کننده 1immediate early gene - ژن فوری اولیهextracellular signal-regulated kinase - کیناز تنظیم شده سیگنال خارج سلولی
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Extracellular signal-regulated kinases and activator protein 1 transcription factor have been functionally linked to addiction. It has also been shown that extracellular signal-regulated kinase activation can regulate cocaine-induced expression of c-Fos and FosB, two possible components of activator protein 1. A direct link between extracellular signal-regulated kinases and activator protein 1 activation has, however, remained unexplored. In this study, we investigated the role of extracellular signal-regulated kinases in the regulation of DNA-binding activity and composition of activator protein 1 induced in the mouse caudate putamen by cocaine treatment. We have found that pre-treatment with SL327, a selective inhibitor the extracellular signal-regulated kinase pathway, has no influence on cocaine-induced DNA-binding activity of activator protein 1, when examined one hour after an acute cocaine treatment. This phenomenon results from simultaneous decrease of c-Fos protein level and increases in JunB and deltaFosB protein levels. SL327 pre-treatment, however, reduces the DNA-binding activity of the activator protein 1 complex induced six hours after an acute cocaine treatment as well as one hour after the last of the chronic cocaine injections, a phenomenon that results from the concomitant reduction of all cocaine-induced proteins (c-Fos, FosB, ÎFosB, JunB). In conclusion, we have found that extracellular signal-regulated kinase inhibition may not only interfere with cocaine-induced gene expression and activator protein 1 complex activation, but may also disturb the time-course of gene expression and composition of activator protein 1 complex. Our results support the notion that inhibitors of the extracellular signal-regulated kinase pathway could be valuable tools to obliterate cocaine-induced molecular changes and the development of addiction.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 137, Issue 1, 2006, Pages 253-264
Journal: Neuroscience - Volume 137, Issue 1, 2006, Pages 253-264
نویسندگان
K. Radwanska, E. Valjent, J. Trzaskos, J. Caboche, L. Kaczmarek,