Histone Deacetylase Inhibitor Prevents Memory Impairment by Methiothepin

Zuzina, Alena B.; Vinarskaya, Aliya; Balaban, Pavel M.; Roshchin, Matvey

doi:10.1007/978-3-030-71637-0_71

Cited by 5 publications

(1 citation statement)

References 49 publications

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“…HDACis NaB or TSA prevented the weakening of potentiation, in other words, they rescued the synaptic plasticity de cit. These results are fully consistent with our previous study in which simultaneous administration of histone deacetylase inhibitor sodium butyrate and a blocker of serotonin receptors methiothepin under conditions of memory reactivation prevented weakening of the context memory in mollusks (Zuzina et al 2021). Similar ability of HDACis to act as a cognitive enhancers was demonstrated in a number of earlier works In a separate series of experiments, we examined how the HDAC inhibition affects synaptic plasticity induced by the weak training protocols.…”

Section: Discussionsupporting

confidence: 91%

Contribution of histone acetylation to the serotonin-mediated long-term synaptic plasticity in terrestrial snails

Zuzina

Balaban

2022

J Comp Physiol A

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Serotonin plays a decisive role in long-term synaptic plasticity and long-term memory in mollusks.Previously, we demonstrated that histone acetylation is a critical regulatory mechanism of long-term memory in terrestrial snail. At the behavioral level, many studies were done in Helix to elucidate the role of histone acetylation and serotonin. However, the impact of histone acetylation on long-term potentiation of synaptic e ciency in electrophysiological studies in Helix has been studied only in one paper. Here we investigated effects of serotonin, histone deacetylases inhibitors sodium butyrate and trichostatin A, and a serotonergic receptor inhibitor methiothepin on long-term potentiation of synaptic responses in vitro. We demonstrated that long-term potentiation was suppressed by methiothepin but rescued by coapplication of histone deacetylase inhibitors sodium butyrate or trichostatin A. Increased histone acetylation compensated the loss of serotonergic activation. We showed that single serotonin application in combination with histone deacetylase blockade could mimic the effect of repeated serotonin applications and be enough for sustained long-lasting synaptic changes. The data obtained demonstrated that histone deacetylases blockade ameliorated de cits in synaptic plasticity induced by different paradigms (methiothepin treatment, the weak training protocol with single application of serotonin), suggesting that histone acetylation contributes to the serotonin-mediated synaptic plasticity.

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Section: Discussionsupporting

confidence: 91%