scholarly journals Chronic Administration of Benzo(a)pyrene Induces Memory Impairment and Anxiety-Like Behavior and Increases of NR2B DNA Methylation

PLoS ONE ◽  
2016 ◽  
Vol 11 (2) ◽  
pp. e0149574 ◽  
Author(s):  
Wenping Zhang ◽  
Fengjie Tian ◽  
Jinping Zheng ◽  
Senlin Li ◽  
Mei Qiang
2021 ◽  
Author(s):  
Lamis Saad ◽  
Andries Kalsbeek ◽  
Jean Zwiller ◽  
Patrick Anglard

Abstract The circadian system interacts with the mesocorticolimbic reward system to modulate reward and memory in a time-of-day dependent manner. The circadian discrimination of reward however remains difficult to address between natural reinforcers and drugs of abuse. Circadian rhythms control cocaine sensitization and conversely cocaine causes long-term alteration in circadian periodicity in part through the serotonergic neurotransmission. Since neural circuits activated by cocaine and natural reinforcers do not completely overlap, we compared the effect of cocaine with that of sucrose, a strong reinforcer in rodents, by using passive chronic administration. The expression of fifteen genes playing a major role in DNA methylation (Dnmts, Tets), circadian rhythms (Clock, Bmal1, Per1/2, Cry1/2, Rev-Erbβ, Dbp1), appetite and satiety (Orexin, Npy) was analyzed in dopamine projection areas like the prefrontal cortex, the caudate putamen, and the hypothalamus interconnected with the reward system. The corresponding proteins of two genes (Orexin, Per2) were examined by IHC. For many factors controlling various biological functions, striking opposite responses were found between the two reinforcers. Global DNA methylation analysis showed that cocaine increased, while sucrose decreased the cytosine methylation content. The data are consistent with a repression of critical core-clock genes by cocaine, suggesting that consequently both agents differentially modulate day/night cycles. Whether cocaine-induced changes are long lasting, or contribute to the establishment of drug addiction requires further neuroepigenetic investigation. Understanding the mechanisms dissociating drugs of abuse from natural reinforcers remains a prerequisite for the design of selective therapeutic tools for compulsive behaviors.


2020 ◽  
Vol 10 (1) ◽  
Author(s):  
M. Konki ◽  
N. Lindgren ◽  
M. Kyläniemi ◽  
R. Venho ◽  
E. Laajala ◽  
...  

2018 ◽  
Vol 25 (4) ◽  
pp. 191-200 ◽  
Author(s):  
Rahul Kumar ◽  
Vishal Jain ◽  
Neetu Kushwah ◽  
Aastha Dheer ◽  
Kamla Prasad  Mishra ◽  
...  

Neuroreport ◽  
2018 ◽  
Vol 29 (13) ◽  
pp. 1099-1103 ◽  
Author(s):  
Jue He ◽  
Fan Liu ◽  
Qian Zu ◽  
Zhizhong Xu ◽  
Huifei Zheng ◽  
...  

2021 ◽  
pp. 1-10
Author(s):  
Quan Feng Liu ◽  
Suganya Kanmani ◽  
Jinhyuk Lee ◽  
Geun-Woo Kim ◽  
Songhee Jeon ◽  
...  

Background: Alzheimer’s disease (AD) is the most general, chronic, and progressive neurodegenerative senile disorder characterized clinically by progressive cognitive deterioration and memory impairment. Neoline is effective against neuropathic pain models, but the effects of neoline against AD-like phenotypes have not been investigated. Objective: We offer the investigation of the effects of neoline in AD. Methods: In this study, a Tg-APPswe/PS1dE9 AD mouse model was treated orally with neoline at a concentration of 0.5 mg/kg or 0.1 mg/kg starting at 7.5 months and administered for three months, and its anti-AD effects were evaluated. Results: Neoline improved memory and cognition impairments and reduced the number of amyloid-beta plaque and the amount of amyloid-β in the brain of AD mice. Furthermore, neoline reduced the anxiety behavior in the AD mouse model. The chronic administration of neoline also induced AMPK phosphorylation and decreased tau, amyloid-β, and BACE1 expression in the hippocampus. These findings indicate that chronic administration of neoline has therapeutic effects via AMPK activation, and BACE1 downregulation resulted in a decrease in the amyloid-β levels in the brain of Tg-APPswe/PS1dE9 AD mice. Conclusion: Our results suggest that neoline is a therapeutic agent for the cure of neurodegenerative diseases like AD.


Life Sciences ◽  
2006 ◽  
Vol 79 (23) ◽  
pp. 2209-2216 ◽  
Author(s):  
Asif R. Pathan ◽  
Bhoomi Viswanad ◽  
Swapnil K. Sonkusare ◽  
Poduri Ramarao

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