This study was a prospective examination of tobacco withdrawal symptoms in a controlled environment. Smokers (N=27) were hospitalized for a 7-day period during which a battery of tests was administered. Smokers were assigned to either an experimental group (N=20) or a control group (N=7). Subjects in the experimental group smoked ad libitum for a 3-day baseline period and then underwent 4 days of tobacco deprivation. Subjects in the control group continued to smoke ad libitum throughout the study. Of the 37 measures of tobacco withdrawal employed in this study, nine showed significant changes following tobacco deprivation. These changes include decreased heart rate and increased caloric intake, weight, craving for tobacco, confusion, depression-dejection, number of awakenings, duration of awakenings, and increased poor concentrations as observed by others.
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"Increased consumption of sweet-tasting and high-caloric food is one consequence of withdrawal in human alcoholics (Junghanns et al. 2000; for review, see Kampov-Polevoy et al. 1999) and smokers (Grunberg 1982; Hall et al. 1989; Hatsukami et al. 1984, 1993) as well as in nicotine-dependent laboratory animals (Grunberg et al. 1985, 1988a, b). A suggested explanation for this phenomenon has been that nicotine as well as alcohol withdrawal increases plasma levels of insulin (Grunberg et al. 1985, 1988a; Passilta et al. 1999). "
[Show abstract][Hide abstract] ABSTRACT: We recently demonstrated that blocking specific nicotinic acetylcholine receptors (nAChRs) abolishes the conditioned reinforcing properties of ethanol-associated cues in rat, suggesting nAChRs as promising pharmacological targets for prevention of cue-induced relapse.
The present study investigated the involvement of nAChR subtypes in the conditioned reinforcing properties of stimuli associated with a natural reward (sucrose).
Water-deprived rats were trained to associate a tone + light stimulus (CS) with the presentation of a 0.1 M sucrose solution for 10 consecutive days. On the subsequent day, the animals were tested on the stringent acquisition of a new instrumental response with conditioned reinforcement, following a systemic injection of the nonselective nAChR antagonist mecamylamine (MEC) or the selective α7 and α6/α3β2β3* nAChR antagonist methyllycaconitine (MLA). At testing, the rats were presented with two novel levers. Responding on the lever assigned as active (CR lever) resulted in a presentation of the CS alone, while pressing the inactive lever (NCR lever) had no programmed consequences.
Control animals pressed the CR lever significantly more than the NCR lever, demonstrating that the CR had acquired conditioned reinforcing properties. Systemic MEC as well as MLA reduced the CR lever responses to the same level as for the NCR lever.
These results demonstrate a role for the α7 and/or α6/α3β2β3* nAChRs in conditioned reinforcement to a natural reward and suggest neuronal nAChRs as common mediators of the impact of cues on incentive processes.
"The severity of nicotine dependence was assessed using the FTND (Heatherton et al. 1991) at intake only. Nicotine withdrawal symptoms were assessed using the Minnesota Withdrawal Questionnaire (MWQ; Hatsukami et al. 1984), and craving was assessed using the Tiffany Smoking Urges Questionnaire (Tiffany & Drobes, 1991) on SPECT scan day pre-and post-nicotine inhaler challenge. Two factors of Tiffany Smoking Urges Questionnaire were employed here: desire (positive symptoms associated with wanting a cigarette ; e.g. "
[Show abstract][Hide abstract] ABSTRACT: The Nicotrol® (Pfizer, USA) nicotine inhaler reduces craving by mimicking the behavioural component of cigarettes and delivering controlled doses of nicotine, which binds to the beta-2 subunit-containing nicotinic acetylcholine receptors (β2*-nAChRs). Previous studies examined β2*-nAChR occupancy after administration of regular and low-nicotine cigarettes. Here, we measured occupancy of β2*-nAChRs after administration of nicotine via inhaler, and the relationship between occupancy and changes in craving for tobacco smoking and withdrawal symptoms. Tobacco smokers participated in [123I]5-IA-85380 SPECT studies with either a nicotine inhaler (n=9) or tobacco cigarette (n=4) challenge. [123I]5-IA was administered as a bolus plus constant infusion. After equilibrium was achieved, three 30-min baseline scans were collected, and subjects either used the nicotine inhaler or a regular cigarette, and up to six additional scans were obtained. Receptor occupancy was determined based on the Lassen plot method. Craving for tobacco smoking and withdrawal symptoms were evaluated pre- and post-challenge. Use of the nicotine inhaler produced an average 55.9±6.4% occupancy of β2*-nAChRs 2-5 h post-challenge, whereas use of a cigarette produced significantly higher receptor occupancy (F=10.6, p=0.009) with an average 67.6±14.1% occupancy 1.5-5 h post-challenge. There was a significant decrease in withdrawal symptoms post-nicotine inhaler use (F=6.13, p=0.04). These results demonstrate significant differences in occupancy of β2*-nAChRs by nicotine after use of the inhaler vs. a cigarette and confirm the ability of the nicotine inhaler to relieve withdrawal symptoms.
The International Journal of Neuropsychopharmacology 10/2010; 14(3):389-98. DOI:10.1017/S1461145710001227 · 4.01 Impact Factor
"A number of available human laboratory models have been designed to investigate the various aspects of smoking behavior and nicotine-dependence phenomena (see Lerman et al. 2007 for review) including nicotine discrimination (Perkins et al. 1997, 1999), nicotine reinforcement and tolerance (Perkins et al. 2001, 2002), deprivation effects (Hatsukami et al. 1984) and selfadministration behavior (Hatsukami et al. 1998; Perkins et al. 1997). Probably the best studied human laboratory paradigm examining smoking behavior is the cue-reactivity paradigm. "
[Show abstract][Hide abstract] ABSTRACT: Use of human laboratory analogues of smoking behavior can provide an efficient, cost-effective mechanistic evaluation of a medication signal on smoking behavior, with the result of facilitating translational work in medications development. Although a number of human laboratory models exist to investigate various aspects of smoking behavior and nicotine dependence phenomena, none have yet modeled smoking lapse behavior. The first instance of smoking during a quit attempt (i.e. smoking lapse) is highly predictive of relapse and represents an important target for medications development. Focusing on an abstinence outcome is critical for medication screening as the US Food and Drug Administration approval for cessation medications is contingent on demonstrating effects on smoking abstinence. This paper outlines a three-stage process for the development of a smoking lapse model for the purpose of medication screening. The smoking lapse paradigm models two critical features of lapse behavior: the ability to resist the first cigarette and subsequent ad libitum smoking. Within the context of the model, smokers are first exposed to known precipitants of smoking relapse (e.g. nicotine deprivation, alcohol, stress), and then presented their preferred brand of cigarettes. Their ability to resist smoking is then modeled and once smokers 'give in' and decide to smoke, they participate in a tobacco self-administration session. Ongoing and completed work developing and validating these models for the purpose of medication screening is discussed.