Persistent cognitive and affective alterations at late withdrawal stages after long-term intermittent exposure to tobacco smoke or electronic cigarette vapour: Behavioural changes and their neurochemical correlates

Ponzoni, Luisa; Braida, Daniela; Carboni, Lucia; Moretti, Milena; Viani, Paola; Clementi, Francesco; Zoli, Michèle; Gotti, Cecilia; Sala, Mariaelvina

doi:10.1016/j.phrs.2020.104941

Cited by 15 publications

(9 citation statements)

References 84 publications

(118 reference statements)

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“…Also, tobacco smoke, nicotine vapor, or e-cig aerosol exposed rats that were treated with mecamylamine showed precipitated nicotine withdrawal symptoms, including somatic withdrawal signs and depressive-like behavior (anhedonia) (Chellian et al, 2020;Gilpin et al, 2014;Montanari et al, 2020;Small et al, 2010). Cessation of tobacco smoke and e-cig aerosol after seven weeks of exposure in mice leads to somatic withdrawal signs, learning and memory deficits, and anxiety-and depressive-like behavior (Ponzoni et al, 2015(Ponzoni et al, , 2020. In rats, cessation of a brief period of nicotine vapor exposure (one and 10 days) produces somatic withdrawal signs (Montanari et al, 2020).…”

Section: Role Of Cotinine In the Development Of Nicotine Dependencementioning

confidence: 99%

“…Cessation of tobacco smoke and e-cig aerosol exposure in mice produces long-lasting withdrawal symptoms. Learning and memory deficits, anxiety-and depressive-like behaviors last from day 1 to 90 days after cessation of smoke or e-cig aerosol exposure in mice (Ponzoni et al, 2015(Ponzoni et al, , 2020 (Figure 4). In a recent study by our group, mecamylamine-precipitated somatic withdrawal signs were observed in male but not in female rats that had been exposed to tobacco smoke for 35 days (Chellian et al, 2020).…”

Section: Role Of Cotinine In the Development Of Nicotine Dependencementioning

confidence: 99%

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Rodent models for nicotine withdrawal

et al. 2021

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Background: Animal models are critical to improve our understanding of the neuronal mechanisms underlying nicotine withdrawal. Nicotine dependence in rodents can be established by repeated nicotine injections, chronic nicotine infusion via osmotic minipumps, oral nicotine intake, tobacco smoke exposure, nicotine vapor exposure, and e-cigarette aerosol exposure. The time course of nicotine withdrawal symptoms associated with these methods has not been reviewed in the literature. Aim: The goal of this review is to discuss nicotine withdrawal symptoms associated with the cessation of nicotine, tobacco smoke, nicotine vapor, and e-cigarette aerosol exposure in rats and mice. Furthermore, age and sex differences in nicotine withdrawal symptoms are reviewed. Results: Cessation of nicotine, tobacco smoke, nicotine vapor, and e-cigarette aerosol exposure leads to nicotine withdrawal symptoms such as somatic withdrawal signs, changes in locomotor activity, anxiety- and depressive-like behavior, learning and memory deficits, attention deficits, hyperalgesia, and dysphoria. These withdrawal symptoms are most pronounced within the first week after cessation of nicotine exposure. Anxiety- and depressive-like behavior, and deficits in learning and memory may persist for several months. Adolescent (4–6 weeks old) rats and mice display fewer nicotine withdrawal symptoms than adults (>8 weeks old). In adult rats and mice, females show fewer nicotine withdrawal symptoms than males. The smoking cessation drugs bupropion and varenicline reduce nicotine withdrawal symptoms in rodents. Conclusion: The nicotine withdrawal symptoms that are observed in rodents are similar to those observed in humans. Tobacco smoke and e-cigarette aerosol contain chemicals and added flavors that enhance the reinforcing properties of nicotine. Therefore, more valid animal models of tobacco and e-cigarette use need to be developed by using tobacco smoke and e-cigarette aerosol exposure methods to induce dependence.

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Section: Role Of Cotinine In the Development Of Nicotine Dependencementioning

confidence: 99%

Section: Role Of Cotinine In the Development Of Nicotine Dependencementioning

confidence: 99%

Rodent models for nicotine withdrawal

et al. 2021

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“…Our study shows a decline in working memory following 8 weeks of CS exposure, which persisted beyond 33 days post-cessation suggesting these neurocognitive impairments may be closer related to pulmonary in ammation elicited by CS rather than nicotine withdrawal symptoms, which have been shown to be fully resolved by 8-days post-nicotine withdrawal. Alongside this, studies have found that CS and e-cigarette cessation for more than 30 days markedly impaired spatial and visual memory [51,52]. Similarly, mice exposed to nicotinefree e-cigarettes have impaired working memory performance, further emphasising that cognitive impairments may still occur without nicotine [53].…”

Section: Discussionmentioning

confidence: 97%

Ebselen Prevents Cigarette Smoke-Induced Cognitive Dysfunction In Mice By Preserving Hippocampal Synaptophysin Expression

Luca

Brassington

Chan

et al. 2021

Preprint

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Background: Cigarette smoking (CS) is the leading cause of chronic obstructive pulmonary disease (COPD). The “spill-over” of pulmonary inflammation into the systemic circulation may damage the brain, leading to cognitive dysfunction. Cessation of CS can improve pulmonary and neurocognitive outcomes, however, its benefit on the neuroinflammatory profile remains uncertain. Here, we investigate how CS exposure impairs neurocognition and whether this can be reversed with CS cessation or an antioxidant treatment. Methods: Male BALB/c mice were exposed CS (9 cigarettes/day for 8 weeks) followed by 4 weeks of CS cessation. Another cohort of CS-exposed mice were co-administrated with a glutathione peroxidase (Gpx) mimetic, ebselen (10mg/kg) or vehicle (5% CM-cellulose). We assessed pulmonary inflammation, spatial and working memory, and the hippocampal microglial, oxidative and synaptic profiles. Results: CS exposure increased lung inflammation which was reduced following CS cessation. CS caused spatial and working memory impairments which were attributed to hippocampal microglial activation and suppression of synaptophysin. CS cessation did not improve memory deficits or alter microglial activation. Ebselen completely prevented the CS-induced working and spatial memory impairments, which was associated with restored synaptophysin expression without altering microglial activation.Conclusion: We were able to model the CS-induced memory impairment and microglial activation seen in human COPD. The preventative effects of ebselen on memory impairment is likely to be dependent on a preserved synaptogenic profile. Cessation alone also appears to be insufficient in correcting the memory impairment, suggesting the importance of incorporating antioxidant therapy to help maximizing the benefit of cessation.

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“…MiceVAPORDot has the potential to be a powerful tool to fill the blank of assessing the behavior during the aerosol exposure procedure. Although previous studies have demonstrated that e-cigarette nicotine exposure could influence the behaviors of mice (Garrett et al, 2021; Grant et al, 2016; Ponzoni et al, 2020) no work have characterized behavioral alterations during smoke exposure. The key obstacle could be animal tracking under the occlusion of e-cigarette aerosols.…”

Section: Discussionmentioning

confidence: 99%

MiceVAPORDot: A novel automated approach for high-throughput behavioral characterization during E-cigarette exposure in mice

Han,

Xu,

et al. 2023

Preprint

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The prosperity of electronic nicotine delivery systems (ENDS) or e-cigarette use has been regarded to lead an increasing risk of nicotine addiction, especially among youth. Understanding and evaluating the behaviors induced by ENDS are fundamental to the study of neuropsychiatric effects of e-cigarettes. However, little is known regarding the behavioral features during e-cigarette exposure in mice. Current behavioral assessments for nicotine addiction are based on nicotine withdrawal-induced anxiety which can be only performed after ENDS exposures. Here we developed MiceVAPORDot, a novel high-throughput tool for automatedin situbehavioral characterization during e-cigarette exposure. The integration of a deep learning-based animal pose tracking method by MiceVAPORDot allows precise characterization on behavioral phenotypes of e-vapor exposed mice, which were unable revealed by traditional evaluation methodology such as conditioned place preference and elevated plus maze tests. The behavioral fingerprints recognized by MiceVAPORDot can be used for high-throughput screening on incentive nature of e-cigarette flavors as well as medications for smoking cessation.

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Persistent cognitive and affective alterations at late withdrawal stages after long-term intermittent exposure to tobacco smoke or electronic cigarette vapour: Behavioural changes and their neurochemical correlates

Cited by 15 publications

References 84 publications

Rodent models for nicotine withdrawal

Rodent models for nicotine withdrawal

Ebselen Prevents Cigarette Smoke-Induced Cognitive Dysfunction In Mice By Preserving Hippocampal Synaptophysin Expression

MiceVAPORDot: A novel automated approach for high-throughput behavioral characterization during E-cigarette exposure in mice

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