scholarly journals Correlation between the epigenetic modification of histone H3K9 acetylation of NR2B gene promoter in rat hippocampus and ethanol withdrawal syndrome

2018 ◽  
Author(s):  
Duan Li ◽  
Yanqing Zhang ◽  
Yanting Zhang ◽  
Qi Wang ◽  
Qin Miao ◽  
...  
Keyword(s):  
Nmda Receptor ◽  
Epigenetic Modification ◽  
Gene Promoter ◽  
Ethanol Exposure ◽  
Ethanol Withdrawal ◽  
Rat Hippocampus ◽  
Expression Levels ◽  
Chronic Ethanol Exposure ◽  
Ethanol Withdrawal Syndrome ◽  
H3k9 Acetylation

Previous studies showed that an epigenetic modification of N-methyl-D-aspartate (NMDA) receptor, especially NMDA receptor 2B subunit (NR2B), was involved in the pathological process of ethanol withdrawal syndrome (EWS). However, the relationship between the epigenetic regulation of the NR2B gene in the rat hippocampus region and EWS were inconsistent. A rat model of chronic ethanol exposure was established. EWS score and the behavioral changes were recorded at different points in time. The NR2B expression levels and the histone H3K9 acetylation level in the NR2B gene promoter region were measured using qRT-PCR, Western blot, immunofluorescence and chromatin immunoprecipitation, respectively. Finally, the relationships between the epigenetic modification of histone H3K9 acetylation of NR2B gene promoter and EWS were examined. Our results showed that the EWS score was increased at 2 h, peaked at 6 h after withdrawal of ethanol, and reduced to the level parallel to the normal control group at day 3 after ethanol withdrawal. The NR2B mRNA expression and protein levels showed similar patterns. Further correlation analyses indicted that both histone H3K9 acetylation in NR2B gene promoter and the expression levels of NR2B were positively associated with EWS. Chronic ethanol exposure may result in epigenetic modification of histone H3K9 acetylation in NR2B gene promoter in rat hippocampus, and the expression levels of NR2B were found to be positively correlated with EWS.

scholarly journals Interaction Between Social Defeat Stress and Chronic Ethanol Exposure on Behaviors During Ethanol Withdrawal and Pro-Inflammatory Cytokines in Mice

2021 ◽  
Vol 2 ◽  
pp. 1-11
Author(s):  
Gessynger Morais-Silva ◽  
Pedro B. Portilho ◽  
Juliana Fernandes-Santos ◽  
Rafaella M. Queiroz ◽  
Simone R. Deconte ◽  
...  
Keyword(s):  
Inflammatory Cytokines ◽  
Social Defeat ◽  
Ethanol Exposure ◽  
Ethanol Withdrawal ◽  
Chronic Ethanol ◽  
Social Defeat Stress ◽  
Chronic Ethanol Exposure ◽  
Pro Inflammatory Cytokines

scholarly journals Withdrawal from Chronic Ethanol Exposure Increases Postsynaptic Glutamate Function of Insular Cortex Projections to the Rat Basolateral Amygdala

2019 ◽  
Author(s):  
Molly M. McGinnis ◽  
Brian C. Parrish ◽  
Brian A. McCool
Keyword(s):  
Synaptic Plasticity ◽  
Negative Affect ◽  
Basolateral Amygdala ◽  
Glutamate Release ◽  
Insular Cortex ◽  
Ethanol Exposure ◽  
Ethanol Withdrawal ◽  
Chronic Ethanol ◽  
Chronic Ethanol Exposure ◽  
Chronic Intermittent Ethanol

AbstractA key feature of alcohol use disorder (AUD) is negative affect during withdrawal, which often contributes to relapse and is thought to be caused by altered brain function, especially in circuits that are important mediators of emotional behaviors. Both the agranular insular cortex (AIC) and the basolateral amygdala (BLA) regulate emotions and are sensitive to ethanol-induced changes in synaptic plasticity. The AIC and BLA are reciprocally connected, however, and the effects of chronic ethanol exposure on this circuit have yet to be explored. Here, we use a combination of optogenetics and electrophysiology to examine the pre- and postsynaptic changes that occur to AIC – BLA synapses following withdrawal from 7- or 10-days of chronic intermittent ethanol (CIE) exposure. While CIE/withdrawal did not alter presynaptic glutamate release probably from AIC inputs, withdrawal from 10, but not 7, days of CIE increased AMPA receptor-mediated postsynaptic function at these synapses. Additionally, NMDA receptor-mediated currents evoked by electrical stimulation of the external capsule, which contains AIC afferents, were also increased during withdrawal. Notably, a single subanesthetic dose of ketamine administered at the onset of withdrawal prevented the withdrawal-induced increases in both AMPAR and NMDAR postsynaptic function. Ketamine also prevented the withdrawal-induced increases in anxiety-like behavior measured using the elevated zero maze. Together, these findings suggest that chronic ethanol exposure increases postsynaptic function within the AIC – BLA circuit and that ketamine can prevent ethanol withdrawal-induced alterations in synaptic plasticity and negative affect.

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