I.P. Pavlov Journal of Higher Nervous ActivityI.P. Pavlov Journal of Higher Nervous ActivityЖурнал высшей нервной деятельности им. И.П. Павлова0044-46773034-5316The Russian Academy of Sciences65206210.31857/S0044467724060033ОБЗОРЫ И ТЕОРЕТИЧЕСКИЕ СТАТЬИReview ArticleThe role of action depolymerization in the changes of inhibitory control during long-term potentiation of excitatory transmission in the rat hippocampusРоль деполимеризации актина в изменении тормозных влияний на долговременную потенциацию возбуждающих синапсов гиппокампа крысKudryashovaI. V.КудряшоваИ. В.
Russian Federation
iv_kudryashova@mail.ruInstitute of Higher Nervous Activity and Neurophysiology RASФедеральное государственное бюджетное учреждение науки «Институт высшей нервной деятельности и нейрофизиологии РАН»1112202474666768602022025Copyright ©; 2024, Russian Academy of SciencesCopyright ©; 2024, Российская академия наук2024Russian Academy of SciencesРоссийская академия наукhttps://innoscience.ru/0044-4677/article/view/652062

The plasticity of inhibitory resposes during CA3-CA1 long-term potentiation (LTP) in the rat hippocampal slices was studied by the method of paired-pulse stimulation. Coefficients of inhibition were estimated by the differences between IPSP dependent and independent paired-pulse plasticity. In the experimental group high frequency stimulation of Schaffer collaterals was delivered under jasplakinolide exposure, this inhibitor of actin depolymerization is used also as activator of actin polymerization. It was shown that the feature of LTP development after induction with blockade of actin depolymerization include altered modification profile of inhibition, specifically involved in resposes to paired-pulse stimulation. Initial enhancement of inhibition depended on the value before tetanization. Therefore this factor may be responsible for between-group differences and it was taken into account in the evaluation of specific for posttetanic depolymerization changes. In result, this phase is related to disinhibition disorder during LTP consolidation and maintenance. It may be assumed that coordinating role of actin cytoskeleton is essential for balanced modifications of excitatory and inhibitory transmission during long-term plasticity.

Для исследования изменения эффективности торможения при долговременной потенциации в поле СА1 переживающих срезов гиппокампа крыс был использован метод парной стимуляции. Коэффициенты торможения вычисляли по соотношению зависимых и независимых от ТПСП реакций. В экспериментальной группе срезов тетанизация коллатералей Шаффера производиласть на фоне джасплакинолида, ингибитора деполимеризации, применяемого также для индукции полимеризации актина. Обнаружено, что особенности развития СА1 LTP при индукции на фоне блокады деполимеризации актина включают изменение динамики модификаций тормозного компонента реакций на парную стимуляцию. Первоначальное усиление торможения зависело от его исходного уровня, и изменения при аппликации джасплакиналида до начала тетанизации могут быть главной причиной межгрупповых различий. Поэтому этот фактор учитывался при анализе изменений, специфичных для блокады ранней фазы деполимеризации актина. Показано, что к ним относится нарушение процесса растормаживания в фазе консолидации и поддержания LTP. Предполагается, что координирующая роль актинового цитоскелета определяет сбалансированность долговременных модификаций возбуждающих и тормозных синапсов.

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