Effect of transdermal nicotine replacement on alcohol responses and alcohol self-administration

Psychopharmacology (Impact Factor: 3.99). 02/2008; 196(2):189-200. DOI: 10.1007/s00213-007-0952-3

ABSTRACT RationaleNicotine replacement is commonly used to treat tobacco use in heavy-drinking smokers. However, few studies have examined the
effect of nicotine replacement on subjective and physiological responses to alcohol and alcohol drinking behavior.

ObjectiveThe primary aim of this within-subject, double-blind study was to examine whether transdermal nicotine replacement (0mg vs
21mg/day) altered response to a low-dose priming drink and subsequent ad libitum drinking behavior.

Materials and methodsSubjects (n = 19) were non-treatment-seeking, non-dependent heavy drinkers who were daily smokers. Six hours after transdermal patch
application, subjective and physiological responses to a priming drink [designed to raise blood alcohol levels (BALs) to 0.03g/dl]
were assessed. This was followed by a 2-h self-administration period where subjects could choose to consume up to eight additional
drinks (each designed to raise BALs by 0.015g/dl) or to receive monetary reinforcement for drinks not consumed.

ResultsWe found that 6h after patch application, tobacco craving associated with withdrawal relief was decreased, and systolic blood
pressure and heart rate were increased in the active patch condition compared to the placebo patch condition. Subjective intoxication
in response to the priming drink was attenuated in the active nicotine patch condition compared to 6h of nicotine deprivation
(i.e., placebo patch). During the self-administration period, subjects had longer latencies to start drinking and consequently
appeared to consume fewer drinks when administered the active patch compared to the placebo patch.

ConclusionsIn heavy drinkers, transdermal nicotine replacement compared to mild nicotine deprivation attenuated subjective and physiological
alcohol responses and delayed the initiation of drinking.

Download full-text


Available from: Stephanie S. O’Malley, Jan 02, 2015
1 Follower
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Alcohol is frequently co-abused with smoking. In humans, nicotine use can increase alcohol craving and consumption. The objectives of the current study were to assess the acute effects of nicotine on alcohol seeking and relapse at 2 different time points. Adult female alcohol-preferring (P) rats were trained in 2-lever operant chambers to self-administer 15% ethanol (EtOH) (v/v) and water on a concurrent fixed-ratio 5-fixed-ratio 1 (FR5-FR1) schedule of reinforcement in daily 1-hour sessions. Following 10 weeks of daily 1-hour sessions, rats underwent 7 extinction sessions, followed by 2 weeks in their home cages. Rats were then returned to the operant chambers without EtOH or water being present for 4 sessions (Pavlovian Spontaneous Recovery [PSR]). Rats were then given a week in their home cage before being returned to the operant chambers with access to EtOH and water (relapse). Nicotine (0, 0.1, 0.3, or 1.0 mg/kg) was injected subcutaneously immediately or 4 hours prior to PSR or relapse testing. Injections of nicotine immediately prior to testing reduced (5 to 10 responses PSR; 50 to 60 responses relapse), whereas injections of nicotine 4 hours prior to testing increased (up to 150 responses for PSR; up to 400 responses for relapse with 1.0 mg/kg dose) responses on the EtOH lever during PSR and relapse tests. The results of this study demonstrate that acute effects of nicotine on EtOH-seeking and relapse behaviors may be time dependent, with the immediate effects being a result of nicotine possibly acting as a substitute for EtOH, whereas with a delay of 4 hours, priming effects of nicotine alterations in nicotinic receptors, and/or the effects of nicotine's metabolites (i.e., cotinine and nornicotine) may enhance the expression of EtOH-seeking and relapse behaviors.
    Alcoholism Clinical and Experimental Research 06/2011; 36(1):43-54. DOI:10.1111/j.1530-0277.2011.01579.x · 3.31 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: This paper reviews evidence suggesting that nicotine and tobacco smoke profoundly modulate the effects of alcohol on γ-aminobutyric acid (GABA) neuronal function, specifically at the GABA(A)-benzodiazepine receptor (GABA(A)-BZR). The focus of this paper is on recent neuroimaging evidence in preclinical models as well as clinical experiments. First, we review findings implicating the role of alcohol at the GABA(A)-BZR and discuss the changes in GABA(A)-BZR availability during acute and prolonged alcohol withdrawal. Second, we discuss preclinical evidence that suggests nicotine affects GABA neuronal function indirectly by a primary action at neuronal nicotinic acetylcholine receptors. Third, we show how this evidence converges in studies that examine GABA levels and GABA(A)-BZRs in alcohol-dependent smokers and nonsmokers, suggesting that tobacco smoking attenuates the chemical changes that occur during alcohol withdrawal. Based on a comprehensive review of literature, we hypothesize that tobacco smoking minimizes the changes in GABA levels that typically occur during the acute cycles of drinking in alcohol-dependent individuals. Thus, during alcohol withdrawal, the continued tobacco smoking decreases the severity of the withdrawal-related changes in GABA chemistry. This article is part of a Special Issue entitled 'Trends in neuropharmacology: in memory of Erminio Costa'.
    Neuropharmacology 06/2011; 60(7-8):1318-25. DOI:10.1016/j.neuropharm.2011.01.020 · 4.82 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Nicotine was reported to reduce the plaque burden and could be used as a possible anti-Alzheimer's disease agent. However, the effect of nicotine on memory and tau pathology in Alzheimer's disease has been less studied. The present study investigated the effect of nicotine on tau phosphorylation and cognitive impairment induced by hippocampus injections of amyloid-beta (Abeta) 25-35. Rats were treated with nicotine hydrogen tartrate salt dissolved in normal saline by subcutaneous injection twice per day for 14 days. The age and gender matched rats treated with same amount of normal saline were used as the control. Morris water maze was used to detect the cognitive impairment induced by Abeta25-35. Compared to the sham-operated rats, Abeta25-35 injection significantly prolonged the mean escape latency in vehicle-treated rats in the Morris water maze test and increased the number of tau(pS202) and tau(pT231) immunoreactive cells. The data show that nicotine (1mg/kg in base weight) treatment significantly exacerbates cognitive impairment and tau phosphorylation at Ser-202 and Thr-231 in the hippocampus compared with Abeta25-35 injection groups in the Abeta rat model of Alzheimer's disease. The use of nicotine for treatment of Alzheimer's disease should be reassessed.
    European journal of pharmacology 04/2010; 637(1-3):83-8. DOI:10.1016/j.ejphar.2010.03.029 · 2.68 Impact Factor