INDUCTION OF ACETYLATION PROCESSES IN ANIMALS WITH SEROTONERGIC NEURON DYSFUNCTION REVERSES THEIR CAPABILITY OF LONG-TERM MEMORY FORMATION

The major tasks of neurobiology include the understanding of mechanisms governing long-term memory formation and search for means to improve memory. Animals with dysfunction of the serotonergic system are a convenient model for investigation of memory processes. The ablation of serotonergic neurons...

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Main Authors: O. V. Vorobiova, L. N. Grinkevich
Format: Article
Language:English
Published: Siberian Branch of the Russian Academy of Sciences, Federal Research Center Institute of Cytology and Genetics, The Vavilov Society of Geneticists and Breeders 2015-01-01
Series:Вавиловский журнал генетики и селекции
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Online Access:https://vavilov.elpub.ru/jour/article/view/257
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author O. V. Vorobiova
L. N. Grinkevich
author_facet O. V. Vorobiova
L. N. Grinkevich
author_sort O. V. Vorobiova
collection DOAJ
description The major tasks of neurobiology include the understanding of mechanisms governing long-term memory formation and search for means to improve memory. Animals with dysfunction of the serotonergic system are a convenient model for investigation of memory processes. The ablation of serotonergic neurons by the neurotoxin 5,7-DOT leads to inability of the mollusks to form an aversive food avoidance reflex. Previously we have found that epigenetic processes, such as histone methylation and acetylation, are involved in the formation of food aversion, and that disturbance of these processes leads to inability to form long-term memory. The goal of the current study was to investigate the possibility to reverse long-term memory in DOT-treated animals through the induction of acetylation processes. We found that treatment with histone deacetylase inhibitors NаB and Trichostatin А significantly increased the ability of DOT-treated animals to form the food aversion reflex. The results point to an important role of serotonin in the induction of the epigenetic processes mediating the formation of this type of long-term memory. By induction of acetylation processes, we managed to improve memory parameters significantly. Our “Neurodegeneration” model, based on ablation of serotonergic neurons, can be useful in studies of the epigenetic mechanisms underlying long-term memory destruction and screening of compounds crucial for memory formation.
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institution Kabale University
issn 2500-3259
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publishDate 2015-01-01
publisher Siberian Branch of the Russian Academy of Sciences, Federal Research Center Institute of Cytology and Genetics, The Vavilov Society of Geneticists and Breeders
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spelling doaj-art-c7f975a3bc344b49a13c0d2eabfa513f2025-02-01T09:58:00ZengSiberian Branch of the Russian Academy of Sciences, Federal Research Center Institute of Cytology and Genetics, The Vavilov Society of Geneticists and BreedersВавиловский журнал генетики и селекции2500-32592015-01-01182345353241INDUCTION OF ACETYLATION PROCESSES IN ANIMALS WITH SEROTONERGIC NEURON DYSFUNCTION REVERSES THEIR CAPABILITY OF LONG-TERM MEMORY FORMATIONO. V. Vorobiova0L. N. Grinkevich1Pavlov Institute of Physiology Russian Academy of Sciences, St. Petersburg, RussiaPavlov Institute of Physiology Russian Academy of Sciences, St. Petersburg, RussiaThe major tasks of neurobiology include the understanding of mechanisms governing long-term memory formation and search for means to improve memory. Animals with dysfunction of the serotonergic system are a convenient model for investigation of memory processes. The ablation of serotonergic neurons by the neurotoxin 5,7-DOT leads to inability of the mollusks to form an aversive food avoidance reflex. Previously we have found that epigenetic processes, such as histone methylation and acetylation, are involved in the formation of food aversion, and that disturbance of these processes leads to inability to form long-term memory. The goal of the current study was to investigate the possibility to reverse long-term memory in DOT-treated animals through the induction of acetylation processes. We found that treatment with histone deacetylase inhibitors NаB and Trichostatin А significantly increased the ability of DOT-treated animals to form the food aversion reflex. The results point to an important role of serotonin in the induction of the epigenetic processes mediating the formation of this type of long-term memory. By induction of acetylation processes, we managed to improve memory parameters significantly. Our “Neurodegeneration” model, based on ablation of serotonergic neurons, can be useful in studies of the epigenetic mechanisms underlying long-term memory destruction and screening of compounds crucial for memory formation.https://vavilov.elpub.ru/jour/article/view/257epigeneticshistone acetylationserotoninmemoryhelix molluskneurotoxin 5,7-dothistone deacetylase inhibitors nab and tca
spellingShingle O. V. Vorobiova
L. N. Grinkevich
INDUCTION OF ACETYLATION PROCESSES IN ANIMALS WITH SEROTONERGIC NEURON DYSFUNCTION REVERSES THEIR CAPABILITY OF LONG-TERM MEMORY FORMATION
Вавиловский журнал генетики и селекции
epigenetics
histone acetylation
serotonin
memory
helix mollusk
neurotoxin 5,7-dot
histone deacetylase inhibitors nab and tca
title INDUCTION OF ACETYLATION PROCESSES IN ANIMALS WITH SEROTONERGIC NEURON DYSFUNCTION REVERSES THEIR CAPABILITY OF LONG-TERM MEMORY FORMATION
title_full INDUCTION OF ACETYLATION PROCESSES IN ANIMALS WITH SEROTONERGIC NEURON DYSFUNCTION REVERSES THEIR CAPABILITY OF LONG-TERM MEMORY FORMATION
title_fullStr INDUCTION OF ACETYLATION PROCESSES IN ANIMALS WITH SEROTONERGIC NEURON DYSFUNCTION REVERSES THEIR CAPABILITY OF LONG-TERM MEMORY FORMATION
title_full_unstemmed INDUCTION OF ACETYLATION PROCESSES IN ANIMALS WITH SEROTONERGIC NEURON DYSFUNCTION REVERSES THEIR CAPABILITY OF LONG-TERM MEMORY FORMATION
title_short INDUCTION OF ACETYLATION PROCESSES IN ANIMALS WITH SEROTONERGIC NEURON DYSFUNCTION REVERSES THEIR CAPABILITY OF LONG-TERM MEMORY FORMATION
title_sort induction of acetylation processes in animals with serotonergic neuron dysfunction reverses their capability of long term memory formation
topic epigenetics
histone acetylation
serotonin
memory
helix mollusk
neurotoxin 5,7-dot
histone deacetylase inhibitors nab and tca
url https://vavilov.elpub.ru/jour/article/view/257
work_keys_str_mv AT ovvorobiova inductionofacetylationprocessesinanimalswithserotonergicneurondysfunctionreversestheircapabilityoflongtermmemoryformation
AT lngrinkevich inductionofacetylationprocessesinanimalswithserotonergicneurondysfunctionreversestheircapabilityoflongtermmemoryformation