Neuroprotective effects of soy isoflavones on chronic ethanol-induced dementia in male ICR mice

2020 ◽  
Vol 11 (11) ◽  
pp. 10011-10021
Author(s):  
Cong Lu ◽  
Rongjing Gao ◽  
Jingwei Lv ◽  
Ying Chen ◽  
Shuying Li ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Synaptic Plasticity ◽  
Cognitive Deficit ◽  
Ethanol Exposure ◽  
Soy Isoflavones ◽  
Chronic Ethanol ◽  
Neuroprotective Effects ◽  
Cholinergic Function ◽  
Chronic Ethanol Exposure ◽  
Neuron Apoptosis

Chronic ethanol intake can lead to cognitive deficit by reducing cholinergic function, inhibiting synaptic plasticity and causing neuron apoptosis. Soy isoflavones effectively improved the cognitive impairment induced by chronic ethanol exposure.

Alterations of Rat Corticostriatal Synaptic Plasticity After Chronic Ethanol Exposure and Withdrawal

2006 ◽  
Vol 30 (5) ◽  
pp. 819-824 ◽  
Author(s):  
Jian Xun Xia ◽  
Jing Li ◽  
Rong Zhou ◽  
Xiao Hu Zhang ◽  
Yin Bing Ge ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Ethanol Exposure ◽  
Chronic Ethanol ◽  
Chronic Ethanol Exposure

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.

Chronic ethanol exposure induces alterations in the nucleocytoplasmic transport in growing astrocytes

2008 ◽  
Vol 106 (4) ◽  
pp. 1914-1928 ◽  
Author(s):  
María Pilar Marín ◽  
Mónica Tomas ◽  
Guillermo Esteban-Pretel ◽  
Luis Megías ◽  
Carmen López-Iglesias ◽  
...  
Keyword(s):  
Nucleocytoplasmic Transport ◽  
Ethanol Exposure ◽  
Chronic Ethanol ◽  
Chronic Ethanol Exposure

Skeletal Toxicity Associated with Chronic Ethanol Exposure in a Rat Model Using Total Enteral Nutrition

2002 ◽  
Vol 301 (3) ◽  
pp. 1132-1138 ◽  
Author(s):  
Elizabeth C. Brown ◽  
Daniel S. Perrien ◽  
Terry W. Fletcher ◽  
David J. Irby ◽  
James Aronson ◽  
...  
Keyword(s):  
Enteral Nutrition ◽  
Rat Model ◽  
Ethanol Exposure ◽  
Chronic Ethanol ◽  
Chronic Ethanol Exposure ◽  
Total Enteral Nutrition
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