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The Effects of Chronic Cigarette Smoke Extract Exposure on Somatic Withdrawal
Author(s) -
Reynaga Daisy,
Leslie Frances,
Belluzzi James
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.1187.1
Subject(s) - nicotine withdrawal , nicotine , mecamylamine , smoking cessation , medicine , somatic cell , pharmacology , self administration , rodent , physiology , nicotinic agonist , receptor , chemistry , pathology , biology , biochemistry , gene , ecology
Tobacco dependence is extremely difficult to treat and the vast majority of those who try to quit will relapse within the first year. Tobacco withdrawal is a major cause of relapse during the first few days of the quitting attempt. Adult rodent models of nicotine exposure show similar symptoms of withdrawal as humans. However, although human adolescents have an increased sensitivity to the effects of smoking cessation, rodent adolescents experience little to no somatic withdrawal symptoms after chronic nicotine exposure (DiFranza et al., 2007; O'Dell, 2009; Torres et al., 2013). This discrepancy may be due to the lack of other non‐nicotine smoke constituents in current animal models. We have shown that rats exposed to aqueous cigarette smoke extract (CSE), a solution containing nicotine and other cigarette smoke constituents, are more sensitive to stress‐induced reinstatement of self‐administration (Costello et al., 2014). The goal of this study is to determine whether adult and adolescents rats show enhanced spontaneous somatic withdrawal symptoms after chronic exposure to CSE, and to investigate the involvement of nicotinic acetylcholine receptors (nAChRs) in CSE cessation‐induced withdrawal using mecamylamine, a nonselective and noncompetitive nAChR antagonist, to precipitate withdrawal. To compare withdrawal effects, adult and adolescent rats were exposed to nicotine or CSE (1.5 mg nicotine/kg/day; i.v) for 10 days and analyzed for spontaneous or precipitated somatic withdrawal. We found that adult rats that received chronic CSE exposure showed enhanced spontaneous somatic withdrawal that emerged sooner than in animals that received chronic nicotine exposure. Adolescent rats showed significant spontaneous somatic withdrawal after chronic CSE exposure but not after nicotine. Mecamylamine (1 mg/kg; s.c.) administration precipitated withdrawal after chronic CSE exposure in both adult and adolescent rats. This provides evidence that non‐nicotine constituents in CSE mediate withdrawal processes, possibly via sensitization of nAChRs. Support or Funding Information Tobacco Related Disease Research Program (TRDRP): 21RT‐0136 National Institute on Drug Abuse (NIDA): 1RO1DA040440‐01