Инд. авторы:	Лисачев П.Д., Пустыльняк В.О., Штарк М.Б.
Заглавие:	Регуляция экспрессии S100B при долговременной потенциации
Библ. ссылка:	Лисачев П.Д., Пустыльняк В.О., Штарк М.Б. Регуляция экспрессии S100B при долговременной потенциации // Российский физиологический журнал им. И.М. Сеченова. - 2014. - Т.100. - № 8. - С.953-963. - ISSN 0869-8139.
Внешние системы:	РИНЦ: 21836103;
Реферат:	eng: In this study, contributions of intracellular regulatory cascades in the induction of S100B expression in rat hippocampal CA1 area during long term posttetanic potentiation (LTP) were estimated. The activation of transcription factor p53 (positive regulator of S100B transcription) by nutlin-3 increased the basal content of S100B mRNA up to 151 % of the control level, which was significantly lower than its content in tetanized slices (280 %). Therefore, p53 seems to be not unique transcription factor upregulating S100B expression during LTP. The inhibitor of Ca 2+/calmodulin-dependent kinases (CaMKs) KN-93 fully blocked the increase of S100B mRNA after tetanization, while KN-92 (inactive analogue of KN-93) was ineffective. The inhibitor of CaMKII and receptor tyrosine kinases K-252a essentially suppressed S100B expression during LTP, the inhibition of MAPK p38 or RSK2 moderately decreased, and the inhibition of MEK1 did not influence S100B mRNA content. Thus, CaMKs play a key role in the induction of S100B expression during LTP. rus: Исследовалась роль внутриклеточных регуляторных каскадов в индукции экспрессии S100B при формировании долговременной посттетанической потенциации (ДПТП) в поле CA1 срезов гиппокампа крыс. Активация транскрипционного фактора p53 (позитивного регулятора транскрипции S100B) с помощью nutlin-3 увеличивала базальный уровень мРНК S100B до 151 % относительно контроля, что было существенно ниже ее содержания в тетанизированных срезах (280 %). Следовательно, p53 - не единственный транскрипционный фактор, регулирующий экспрессию S100B при ДПТП. Ингибитор Са 2+/кальмодулинзависимых киназ (CaMK) KN-93 полностью блокировал увеличение уровня мРНК S100B после тетанизации, а его неактивный аналог KN-92 не влиял на экспрессию S100B. Ингибитор CaMKII и рецепторных тирозинкиназ K-252a существенно подавлял экспрессию S100B при ДПТП, ингибирование MAPK p38 или RSK2 умеренно снижало, а ингибирование MEK1 не влияло на количество мРНК S100B. Таким образом, кальмодулин-киназы играют ключевую роль в индукции экспрессии S100B при ДПТП.
Ключевые слова:	долговременная потенциация; Hippocampal slices; long term potentiation; Ca 2+/calmodulin-dependent kinases; Ca 2+/кальмодулинзависимые киназы; p53; S100b; CA1; срезы гиппокампа;
Издано:	2014
Физ. характеристика:	с.953-963
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