Behavioral and stereological analysis of the prefrontal cortex of rats submitted to chronic alcohol intake

2019 ◽  
Vol 362 ◽  
pp. 21-27 ◽  
Author(s):  
Rafael Conte ◽  
Fernando Vagner Lobo Ladd ◽  
Aliny Antunes Barbosa Lobo Ladd ◽  
Amanda Lopez Moreira ◽  
Luciana Le Sueur-Maluf ◽  
...  
2021 ◽  
Vol 8 ◽  
Author(s):  
Nieves Pizarro ◽  
Elk Kossatz ◽  
Pedro González ◽  
Alba Gamero ◽  
Emma Veza ◽  
...  

Chronic alcohol intake has been shown to disrupt gut microbiota homeostasis, but whether microbiota modulation could prevent behavioral alterations associated with chronic alcohol intake remains unknown. We investigated the effects of synbiotic dietary supplementation on the development of alcohol-related addictive behavior in female and male mice and evaluated whether these effects were associated with changes in bacterial species abundance, short-chain fatty acids, tryptophan metabolism, and neurotransmitter levels in the prefrontal cortex and hippocampus. Chronic intermittent exposure to alcohol during 20 days induced escalation of intake in both female and male mice. Following alcohol deprivation, relapse-like behavior was observed in both sexes, but anxiogenic and cognitive deficits were present only in females. Synbiotic treatment reduced escalation and relapse to alcohol intake in females and males. In addition, the anxiogenic-like state and cognitive deficits observed in females following alcohol deprivation were abolished in mice exposed to synbiotic. Alcohol-induced differential alterations in microbial diversity and abundance in both sexes. In females, synbiotic exposure abrogated the alterations provoked by alcohol in Prevotellaceae UCG-001 and Ruminococcaceae UCG-014 abundance. In males, synbiotic exposure restored the changes induced by alcohol in Akkermansia and Muribaculum uncultured bacterium abundance. Following alcohol withdrawal, tryptophan metabolites, noradrenaline, dopamine, and γ-aminobutyric acid concentrations in the prefrontal cortex and the hippocampus were correlated with bacterial abundance and behavioral alterations in a sex-dependent manner. These results suggested that a dietary intervention with a synbiotic to reduce gut dysbiosis during chronic alcohol intake may impact differently the gut-brain-axis in females and males.


Author(s):  
Lin Ye ◽  
Shuhao Li ◽  
Xiaochen Liu ◽  
Dingang Zhang ◽  
Liliang Li ◽  
...  

Abstract Aims Alcohol abuse induces multiple neuropathology and causes global burden to human health. Prefrontal cortex (PFC) is one of the most susceptible regions to alcohol-induced neuropathology. However, precise mechanisms underlying these effects on PFC remain to be elucidated. Herein, we investigated whether RIP1/RIP3/MLKL-mediated necroptosis was involved in the alcohol-induced PFC injury, and explored the effect that cannabinoid receptors (CBRs) exerted on the neurotoxicity of alcohol. Methods In this study, dynamic development of neuronal necroptosis in the PFC region was monitored after 95% (v/v) alcohol vapor administration for 15 and 30 days, respectively. Selective CBRs agonists or inverse agonists were pretreated according to the experimental design. All the PFC tissues were isolated and further examined by biochemical and histopathological analyses. Results It was found that chronic alcohol exposure increased the protein level of MLKL and also the phosphorylated levels of RIP1, RIP3 and MLKL in a time-dependent manner, all of which indicated the activation of necroptosis signaling. Particularly, compared to astrocytes, neurons from the PFC showed more prototypical necrotic morphology in response to alcohol insults. In parallel, an increased protein level of CB1R was also found after 15 and 30 days alcohol exposure. Administration of specific inverse agonists of CB1R (AM251 and AM281), but not its agonists or CB2R modulators, significantly alleviated the RIP1/RIP3/MLKL-mediated neuronal necroptosis. Conclusion We reported the involvement of RIP1/RIP3/MLKL-mediated necroptosis in alcohol-induced PFC neurotoxicity, and identified CB1R as a critical regulator of neuronal necroptosis that enhanced our understanding of alcohol-induced neuropathology in the PFC.


2009 ◽  
Vol 42 (3) ◽  
pp. 147-151 ◽  
Author(s):  
Sinan Emre ◽  
Zümrüt Yılmaz ◽  
Feral Öztürk ◽  
M. Hanifi Emre

1989 ◽  
Vol 64 (4) ◽  
pp. 356-359 ◽  
Author(s):  
Juha M. Grönroos ◽  
Timo Kaila ◽  
Heikki J. Aho ◽  
Timo J. Nevalainen

1994 ◽  
Vol 46 (2) ◽  
pp. 163-167 ◽  
Author(s):  
Juha M. Grönroos ◽  
Jukka Laine ◽  
Timo Kaila ◽  
Timo J. Nevalainen

2021 ◽  
Author(s):  
Rea Mittal ◽  
Lilly Su ◽  
Devyani Ramgobin ◽  
Ashwani Garg ◽  
Rahul Jain ◽  
...  

Alcohol use disorder (AUD) is highly prevalent and can lead to many cardiovascular complications, including arrhythmias. Chronic alcohol use has a dose-dependent relationship with incidence of atrial fibrillation (AF), where higher alcohol intake (>3 drinks a day) is associated with higher risk of AF. Meanwhile, low levels of chronic alcohol intake (<1 drink a day) is not associated with increased risk of AF. Mechanistically, chronic alcohol intake alters the structural, functional and electrical integrity of the atria, predisposing to AF. Increased screening can help identify AUD patients early on and provide the opportunity to educate on chronic alcohol use related risks, such as AF. The ideal treatment to reduce risk of incident or recurrent AF in AUD populations is abstinence.


2020 ◽  
Vol 43 (11) ◽  
pp. 1197-1206
Author(s):  
Zhenjuan Chen ◽  
Ancheng Wu ◽  
Hongmei Jin ◽  
Fuhui Liu

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