Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10491962 | PMC |
http://dx.doi.org/10.1016/j.gendis.2023.04.016 | DOI Listing |
Genes Dis
March 2024
Biological Anthropology Institute, College of Basic Medical Science, Jinzhou Medical University, Jinzhou, Liaoning 121000, China.
Asian J Psychiatr
May 2022
Department of Histology and Embryology, School of Basic Medicine, Hengyang Medical College, University of South China, 421001 Hunan, China. Electronic address:
J Syst Integr Neurosci
December 2020
Department of Psychiatry, South Texas Veteran Health Care System, Audie L. Murphy Memorial VA Hospital, San Antonio, TX, Long School of Medicine, University of Texas Medical Center, San Antonio, TX, USA.
Background: In face of an American opioid/psychostimulant crisis with overdose fatalities, due, in part, to the COVOD 19 pandemic, we are proposing a paradigm shift in response. Currently, The FDA has approved pharmaceuticals for the treatment of opioids, alcohol, and nicotine but not for psychostimulants or even cannabis.
Proposition: To respond to the deadly overdose issue globally, we are proposing that the FDA embrace, for the treatment and prophylaxis of opioid and psychostimulant abuse, induction of DNA-guided, dopamine homeostasis.
Int J Biochem Cell Biol
July 2018
School of Life Science and Biotechnology, Shanghai Key Laboratory for Reproductive Medicine, Shanghai Jiao Tong University, Shanghai 200240, China. Electronic address:
A new report has shown that nicotine exposure can decrease serum testosterone by apoptosis in Leydig cells; however, in our previous studies, we have almost never observed apoptosis there. The purpose of this study is to ensure whether apoptosis or autophagy in Leydig cells occurred. Our results confirmed again that the concentration of testosterone in the sera of nicotine-treated mice statistically decreased (P < 0.
View Article and Find Full Text PDFBr J Pharmacol
June 2018
School of Biosciences and Medicine, Faculty of Health and Medical Sciences, University of Surrey, Guildford, Surrey, UK.
Background And Purpose: Evidence suggests that exercise decreases nicotine withdrawal symptoms in humans; however, the mechanisms mediating this effect are unclear. We investigated, in a mouse model, the effect of exercise intensity during chronic nicotine exposure on nicotine withdrawal severity, binding of α4β2*, α7 nicotinic acetylcholine (nAChR), μ-opioid (μ receptors) and D dopamine receptors and on brain-derived neurotrophic factor (BDNF) and plasma corticosterone levels.
Experimental Approach: Male C57Bl/6J mice treated with nicotine (minipump, 24 mg·kg ·day ) or saline for 14 days underwent one of three concurrent exercise regimes: 24, 2 or 0 h·day voluntary wheel running.
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!