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New Insights into the Mechanisms of Action of Cotinine and its Distinctive Effects from Nicotine
dc.contributor.author | Grizzell J.A. | |
dc.contributor.author | Echeverria V. | |
dc.date.accessioned | 2020-09-02T22:19:28Z | |
dc.date.available | 2020-09-02T22:19:28Z | |
dc.date.issued | 2014 | |
dc.identifier | 10.1007/s11064-014-1359-2 | |
dc.identifier.citation | 40, 10, 2032-2046 | |
dc.identifier.issn | 03643190 | |
dc.identifier.uri | https://hdl.handle.net/20.500.12728/4751 | |
dc.description | Tobacco consumption is far higher among a number of psychiatric and neurological diseases, supporting the notion that some component(s) of tobacco may underlie the oft-reported reduction in associated symptoms during tobacco use. Popular dogma holds that this component is nicotine. However, increasing evidence support theories that cotinine, the main metabolite of nicotine, may underlie at least some of nicotine’s actions in the nervous system, apart from its adverse cardiovascular and habit forming effects. Though similarities exist, disparate and even antagonizing actions between cotinine and nicotine have been described both in terms of behavior and physiology, underscoring the need to further characterize this potentially therapeutic compound. Cotinine has been shown to be psychoactive in humans and animals, facilitating memory, cognition, executive function, and emotional responding. Furthermore, recent research shows that cotinine acts as an antidepressant and reduces cognitive-impairment associated with disease and stress-induced dysfunction. Despite these promising findings, continued focus on this potentially safe alternative to tobacco and nicotine use is lacking. Here, we review the effects of cotinine, including comparisons with nicotine, and discuss potential mechanisms of cotinine-specific actions in the central nervous system which are, to date, still being elucidated. © 2014, Springer Science+Business Media New York (outside the USA). | |
dc.language.iso | en | |
dc.publisher | Springer New York LLC | |
dc.subject | Cotinine | |
dc.subject | Nicotine | |
dc.subject | Nicotinic receptors | |
dc.subject | Synaptophysin | |
dc.subject | Tobacco | |
dc.subject | cotinine | |
dc.subject | nicotine | |
dc.subject | antidepressant agent | |
dc.subject | cotinine | |
dc.subject | nicotine | |
dc.subject | nicotinic receptor | |
dc.subject | antidepressant activity | |
dc.subject | blood brain barrier | |
dc.subject | brain development | |
dc.subject | brain function | |
dc.subject | brain region | |
dc.subject | cognition | |
dc.subject | drug half life | |
dc.subject | drug mechanism | |
dc.subject | drug self administration | |
dc.subject | emotion | |
dc.subject | estrogen metabolism | |
dc.subject | executive function | |
dc.subject | human | |
dc.subject | long term potentiation | |
dc.subject | maximum plasma concentration | |
dc.subject | memory | |
dc.subject | nerve cell plasticity | |
dc.subject | nervous system function | |
dc.subject | neurotransmission | |
dc.subject | nonhuman | |
dc.subject | priority journal | |
dc.subject | Review | |
dc.subject | tobacco consumption | |
dc.subject | animal | |
dc.subject | Cognition Disorders | |
dc.subject | drug effects | |
dc.subject | metabolism | |
dc.subject | Animals | |
dc.subject | Antidepressive Agents | |
dc.subject | Cognition | |
dc.subject | Cognition Disorders | |
dc.subject | Cotinine | |
dc.subject | Humans | |
dc.subject | Nicotine | |
dc.subject | Receptors, Nicotinic | |
dc.title | New Insights into the Mechanisms of Action of Cotinine and its Distinctive Effects from Nicotine | |
dc.type | Review |