Abstract

Recently, substantial amount of data has been accumulated in the literature, suggesting an important role of epigenetics in the formation of long-term synaptic plasticity as the main cellular mechanism of learning and memory. In this work, we studied the effect of inhibition of histone deacetylases, one of the types of epigenetic modifications, on the formation of long-term potentiation (LTP) of synaptic responses in premotor (command) neurons responsible for avoidance behavior in grape snails. Potentiation of synaptic inputs in these neurons underlies aversive memory in this animal. We showed that the histone deacetylase inhibitor sodium butyrate increases the amplitude of LTP caused by five tetanizations of the sensory nerve, combined with applications of serotonin. We also found that application of sodium butyrate per se causes an increase in the excitatory postsynaptic potential amplitude 4 h after application, although this increase cannot underlie the effect of LTP observed throughout the experiment. Thus, we demonstrated the role of histone modifications in the mechanisms of synaptic plasticity.

中文翻译：

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组蛋白去乙酰化酶抑制剂增强葡萄蜗牛神经元的长期突触增强

摘要

最近，文献中积累了大量数据，表明表观遗传学在长期突触可塑性的形成中起着重要作用，作为学习和记忆的主要细胞机制。在这项工作中，我们研究了抑制组蛋白去乙酰化酶（一种表观遗传修饰）对葡萄蜗牛中负责回避行为的前运动（命令）神经元突触反应长期增强 (LTP) 形成的影响。这些神经元中突触输入的增强是该动物厌恶记忆的基础。我们发现组蛋白去乙酰化酶抑制剂丁酸钠增加了由五次感觉神经强直和血清素应用引起的 LTP 幅度。我们还发现应用丁酸钠本身导致应用后 4 小时兴奋性突触后电位振幅增加，尽管这种增加不能成为整个实验中观察到的 LTP 效应的基础。因此，我们证明了组蛋白修饰在突触可塑性机制中的作用。