Altered mRNA Levels of Stress-Related Peptides in Mouse Hippocampus and Caudate-Putamen in Withdrawal after Long-Term Intermittent Exposure to Tobacco Smoke or Electronic Cigarette Vapour

International Journal of Molecular Sciences

Michele Zoli¹  Mariaelvina Sala²  Luisa Ponzoni²  Daniela Braida²  Lucia Carboni³  Cecilia Gotti⁴ 

[1] Center for Neuroscience and Neurotechnology (CfNN), Department of Biomedical, Metabolic and Neural Sciences, University of Modena and Reggio Emilia, 41124 Modena, Italy;Department of Medical Biotechnology and Translational Medicine, Università degli Studi di Milano, 20133 Milan, Italy;Department of Pharmacy and Biotechnology, Alma Mater Studiorum—Università di Bologna, 40126 Bologna, Italy;Institute of Neuroscience, CNR, 20162 Milan, Italy;

关键词: e-cigarette;    nicotine addiction;    addiction models;    nociceptin;    opioid peptides;    opioid receptors;   

DOI  :  10.3390/ijms22020599

来源: DOAJ

【 摘 要 】

Nicotine addiction is a severe public health problem. The aim of this study was to investigate the alterations in key neurotransmissions after 60 days of withdrawal from seven weeks of intermittent cigarette smoke, e-cigarette vapours, or an e-cigarette vehicle. In the nicotine withdrawal groups, increased depressive and anxiety/obsessive–compulsive-like behaviours were demonstrated in the tail suspension, sucrose preference and marble burying tests. Cognitive impairments were detected in the spatial object recognition test. A significant increase in Corticotropin-releasing factor (Crf) and Crf1 mRNA levels was observed, specifically after cigarette withdrawal in the caudate-putamen nucleus (CPu). The nociceptin precursor levels were reduced by cigarette (80%) and e-cigarette (50%) withdrawal in the CPu. The delta opioid receptor showed a significant reduction in the hippocampus driven by the exposure to an e-cigarette solubilisation vehicle, while the mRNA levels doubled in the CPu of mice that had been exposed to e-cigarettes. Withdrawal after exposure to e-cigarette vapour induced a 35% Bdnf mRNA decrease in the hippocampus, whereas Bdnf was augmented by 118% by cigarette withdrawal in the CPu. This study shows that long-term withdrawal-induced affective and cognitive symptoms associated to lasting molecular alterations in peptidergic signalling may determine the impaired neuroplasticity in the hippocampal and striatal circuitry.

【 授权许可】

Unknown