The impact of GABAB receptors and their pharmacological stimulation on cocaine reinforcement and drug-seeking behaviors in a rat model of depression

2020 ◽  
Vol 883 ◽  
pp. 173324
Author(s):  
Kinga Gawlińska ◽  
Joanna Jastrzębska ◽  
Sara Gamberini ◽  
Dawid Gawliński ◽  
Renata Pieniążek ◽  
...  
2020 ◽  
Author(s):  
Hongxia Mei ◽  
Ying Tao ◽  
Tianhao Zhang ◽  
Feng Qi

Abstract Background: Acute lung injury (ALI) and/or acute respiratory distress syndrome (ARDS) are critical life-threatening syndromes characterized by the infiltration of a large number of neutrophils that lead to an excessive inflammatory response. Emodin (Emo) is a naturally occurring anthraquinone derivative and an active ingredient of Chinese medicine. It is believed to have anti-inflammatory effects. In this study, we examined the impact of Emo on the pulmonary inflammatory response and the neutrophil function in a rat model of lipopolysaccharide (LPS)-induced ALI.Results: Treatment with Emo protected rat against LPS-induced ALI. Compared to untreated rat, Emo-treated rat exhibited significantly ameliorated lung pathological changes and decreased tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β). However, Emo has no protective effect on the rat model of acute lung injury with neutrophil deficiency. In addition, treatment with Emo enhanced the bactericidal capacity of LPS-induced neutrophils via the up-regulation of the ability of neutrophils to phagocytize bacteria and generate neutrophil extracellular traps (NETs). Emo also downregulated the neutrophil respiratory burst and the expression of reactive oxygen species (ROS) in LPS-stimulated neutrophils, alleviating the damage of neutrophils to surrounding tissues. Finally, Emo can accelerate the resolution of inflammation by promoting apoptosis of neutrophils. Conclusion: Our results provide the evidence that Emo could ameliorates LPS-induced ALI via its anti-inflammatory action by modulating the function of neutrophils. Emo may be a promising preventive and therapeutic agent in the treatment of ALI.


2011 ◽  
Vol 36 (11) ◽  
pp. 1005-1013 ◽  
Author(s):  
Ender Sener ◽  
Nusen Yuksel ◽  
Demir Kursat Yildiz ◽  
Bulent Yilmaz ◽  
Ozdemir Ozdemir ◽  
...  

2020 ◽  
pp. 65-86
Author(s):  
Noelle C. Anastasio ◽  
Dennis J. Sholler ◽  
Brionna D. Davis-Reyes ◽  
Amanda E. Price ◽  
Michelle A. Land ◽  
...  

Vulnerability to initiate use of psychoactive drugs as well as relapse to drug-seeking in patients with established substance use disorders are precipitated by behavioral disinhibition or impulsivity (a predisposition toward rapid unplanned reactions to stimuli without regard to negative consequences) and attentional bias toward drug cues (cue reactivity). These behavioral phenotypes are not independent mechanistically nor neurobiologically, and preclinical analyses have demonstrated the complex nature of the interactions between these interlocked phenotypic behaviors, including aspects of their shared neurobiology and circuitry. This chapter focuses on impulsivity and drug-seeking behaviors from a preclinical perspective and summarizes studies exploring the impact of substances of abuse in the context of the neurobiology of impulsivity and drug-seeking behaviors in rodents.


2017 ◽  
Vol 45 (4) ◽  
pp. 293-300 ◽  
Author(s):  
Di Liu ◽  
Yexin Liu ◽  
Guochun Chen ◽  
Liyu He ◽  
Chengyuan Tang ◽  
...  

Background: IgA nephropathy (IgAN) has been considered to be the most frequent form of primary glomerulonephritis that occurs worldwide with a variety of factors involved in its occurrence and development. The impact of autophagy in IgAN, however, remains partially unclear. This study was designed to investigate the effects of rapamycin in an IgAN model. Method: After establishing an IgAN rat model, SD rats were divided into 4 groups: control, control + rapamycin, IgAN, IgAN + rapamycin. Proteinuria and the pathological changes and the level of autophagy of kidney were texted. Identify the expression of phosphorylation and total mammalian target of rapamycin (mTOR) and s6k1 as well as cyclin D1 in the kidney of rats through Western blot and immunohistochemistry. Results: With rapamycin treatment, we observed a significant reduction in the progression of proteinuria as well as alleviation of pathological lesions in IgAN rats. Besides, autophagy was inhibited, while the mTOR/S6k1 pathway was activated and expression of cyclin D1 was increased in IgAN. Rapamycin treatment increased autophagy and decreased the expression of cyclin D1. Conclusion: These results may suggest that mTOR-mediated autophagy inhibition may result in mesangial cell proliferation in IgAN.


2019 ◽  
Vol 237 (1) ◽  
pp. 55-68 ◽  
Author(s):  
Elizabeth A. Crummy ◽  
Elizabeth A. Donckels ◽  
Britahny M. Baskin ◽  
Brandon S. Bentzley ◽  
Susan M. Ferguson

PLoS ONE ◽  
2014 ◽  
Vol 9 (10) ◽  
pp. e109219 ◽  
Author(s):  
Romeo Teodor Cristina ◽  
Flavia Hanganu ◽  
Eugenia Dumitrescu ◽  
Florin Muselin ◽  
Monica Butnariu ◽  
...  

2016 ◽  
Vol 195 (4S) ◽  
Author(s):  
Tsuyoshi Majima ◽  
Pradeep Tyagi ◽  
Koji Dogishi ◽  
Mahendara Kashyap ◽  
Momokazu Gotoh ◽  
...  

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