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Experimental and Clinical Psychopharmacology - Vol 20, Iss 1

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Experimental & Clinical Psychopharmacology Experimental and Clinical Psychopharmacology seeks to promote the discipline of psychopharmacology in its fullest diversity. Psychopharmacology necessarily involves behavioral change, psychological processes, or their physiological substrates as one central variable and psychopharmacological agents as a second central variable. Such agents will include drugs, medications, and chemicals encountered in the workplace or environment.
Copyright 2012 American Psychological Association
  • 2012 Experimental and Clinical Psychopharmacology.
    The mission of Experimental and Clinical Psychopharmacology has always been to publish scientifically excellent research on psychopharmacology and substance abuse, with an emphasis on translational and interdisciplinary research. The new editor of the journal is introduced in this editorial. She also explains her specific goals for her tenure. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
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  • Contributions of neuroimaging to understanding sex differences in cocaine abuse.
    A consistent observation in drug abuse research is that males and females show differences in their response to drugs of abuse. In order to understand the neurobiology underlying cocaine abuse and effective treatments, it is important to consider the role of sex differences. Sex hormones have been investigated in both behavioral and molecular studies, but further evidence addressing drug abuse and dependence in both sexes would expand our knowledge of sex differences in response to drugs of abuse. Neuroimaging is a powerful tool that can offer insight into the biological bases of these differences and meet the challenges of directly examining drug-induced changes in brain function. As such, neuroimaging has drawn much interest in recent years. Specifically, positron emission tomography (PET), single photon emission computed tomography (SPECT), and magnetic resonance imaging (MRI) technology have emerged as effective noninvasive approaches for human and animal models. Studies have revealed sex-specific changes in patterns of brain activity in response to acute cocaine injection and after prolonged cocaine use. SPECT and PET studies have demonstrated changes in the dopamine transporter but are less clear on other components of the dopaminergic system. This review highlights contributions of neuroimaging toward understanding the role of sex differences in the drug abuse field, specifically regarding cocaine, and identifies relevant questions that neuroimaging can effectively address. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
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  • Exploratory studies in sensory reinforcement in male rats: Effects of methamphetamine.
    Understanding sensory reinforcement and the effects of stimulant drugs on sensory reinforcers is potentially important for understanding their influence on addiction processes. Experiment 1 explored the reinforcing properties of a visual stimulus and the effects of methamphetamine (METH) on responding maintained by a visual reinforcer (VRF) in male rats. Snout poke responses to the active alternative produced the VRF according to variable interval (VI) schedules of reinforcement, and responses to an inactive alternative had no programmed effect. Experiment 2 explored the effects of METH on choice between the VRF and a water reinforcer (H2ORF) using concurrent VI schedules in male rats. In Experiment 1, response-contingent onset of the VRF produced an increase in both the relative frequency and absolute rate of active responding. The rate of both active and inactive responding declined across the 40-min test sessions. METH did not differentially enhance active responding for the VRF. Instead, METH nondifferentially increased the rate of responding and attenuated the within-session decline of responding. In Experiment 2, METH differentially increased the rate of responding for the VRF relative to the H2ORF. The results of these exploratory experiments indicate that the reinforcing effects of the VRF were weak and transient. In addition, METH treatment increased responding, and the specificity of the enhancement of METH was dependent upon the testing conditions. Potential explanations of these differences, such as novelty and reinforcer type, are discussed. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
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  • Acute effects of zolpidem extended-release on cognitive performance and sleep in healthy males after repeated nightly use.
    The extended-release formulation of zolpidem (Ambien CR) is approved for the treatment of insomnia without a treatment duration limit. Acutely zolpidem impairs performance, and no research to date has examined whether tolerance develops to these performance impairments during nighttime awakening. The present double-blind, placebo-controlled study examined whether tolerance develops to zolpidem-induced acute performance impairment after repeated (22–30 days) nightly use. Effects of bedtime administration of zolpidem extended-release (ZOL; 12.5 mg) were tested on a battery of performance measures assessed during a forced nighttime awakening in 15 healthy male volunteers who completed overnight polysomnographic recording sessions in our laboratory at baseline and after approximately a month of at-home ZOL. As expected, bedtime ZOL administration was associated with changes in sleep architecture and impairments across all performance domains during nighttime testing (psychomotor function, attention, working memory, episodic memory, metacognition) with no residual next morning impairment. Tolerance did not develop to the observed ZOL-related impairments on any outcome. Possible evidence of acute abstinence effects after discontinuation of ZOL was observed on some performance and sleep outcomes. Overall, these findings suggest that performance is significantly impaired during nighttime awakening even after a month of nightly ZOL administration, and these impairments could significantly impact safety should nighttime awakening require unimpaired functioning (e.g., driving; combat-related activities in the military). (PsycINFO Database Record (c) 2012 APA, all rights reserved)
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  • Genetic predictors of cue- and stress-induced cigarette craving: An exploratory study.
    Cigarette cravings in response to environmental cues and stressors are widely recognized as important predictors of smoking cessation outcomes. Accumulating evidence suggests that genetics plays a role in these craving responses, as well as in smoking cessation more generally. Previous studies of genetic polymorphisms have been limited by examination of single candidate genes and the use of broadly defined phenotypes (e.g., smoking history). In addition, research examining the similarities and differences between cue- and stress-induced cravings has been limited, although some evidence has suggested that they may have common genetic underpinnings. In the current study, we examined associations between a panel of 1,350 candidate genetic polymorphisms and craving responses to laboratory smoking cues and stressors. We hypothesized that common genetic polymorphisms would be predictive of both cue- and stress-induced craving. Nicotine-dependent smokers (n = 210) donated a blood sample, were exposed to neutral, smoking-related, and stress-related stimuli, and completed craving questionnaires immediately prior to and following each stimulus. Findings indicated that craving responses to smoking cues and stressors were moderately correlated (r = .44). However, genetic analysis revealed that cue and stress-induced cigarette craving were predicted by different polymorphisms, such that variants in the glycine and dopamine pathways were predictive of cue-induced craving, whereas variants in the stress-corticotropin pathway predicted stress-induced craving. Conclusions: Study results provide no support for the hypothesis that cue- and stress-induced craving have the same genetic predictors. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
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  • Exposure to negative affect cues and urge to smoke.
    While much of the cue exposure literature for cigarette smoking has focused on external cues, little has been done in the area of exposing participants to internal cues, such as negative affect (NA), despite the important role of such cues in maintaining smoking behavior. Smokers were exposed to an NA mood induction to induce an urge to smoke and then exposed to NA cues over several trials in an attempt to decrease this urge. Participants (N = 32) were undergraduate smokers assigned to either the exposure or control group for the mood induction procedure, which occurred over 8 trials. All participants viewed NA images and listened to NA music at Trial 1. The exposure group continued to view NA images and listened to NA music, and the control group viewed neutral images and listened to neutral music for 6 subsequent trials lasting about 5 min each. Both groups were exposed to NA images and NA music at Trial 8. NA and urge to smoke ratings were assessed at the end of each trial; heart rate was measured continuously. Results indicated that the mood induction procedure induced NA and urge to smoke, but the extinction procedure did not decrease urge over trials. Heart rate data were not associated with self-report data. In conclusion, the mood induction procedure in the present study appears to be an efficient way to induce urge to smoke. However, further research is necessary to determine why urge to smoke seems to be resistant to extinction. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
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  • Is self-efficacy for smoking abstinence a cause of, or a reflection on, smoking behavior change?
    Social learning theory considers self-efficacy as a causal factor in behavior change. However, in line with behavioral theory, recent clinical research suggests self-efficacy ratings may reflect, rather than cause, behavior change. To test these two disparate views, self-efficacy was related to actual smoking abstinence on the next day (i.e., self-efficacy causes change), and abstinence status over 1 day was tested as a predictor of rated self-efficacy for quitting the next day (i.e., reflects change). All data were from two similar crossover studies evaluating the short-term effects of both placebo versus medication, nicotine patch (n = 209) or varenicline (n = 123), on smoking abstinence during week-long practice quit attempts. Placebo and active medication periods were separated by an ad lib smoking washout, and analyses were controlled for prior-day's abstinence or self-efficacy values. Results were very consistent between studies in showing essentially bidirectional associations: daily self-efficacy predicted next-day's abstinence, and current-day's abstinence status predicted self-efficacy for abstinence the next day. However, secondary factors differentially predicted abstinence and, to a lesser extent, self-efficacy, between these two medication studies. These data provide some support for both social learning and behavioral theories of smoking behavior change, although self-efficacy may only briefly predict subsequent short periods of abstinence as assessed in these studies. Nonetheless, because self-efficacy has long been assumed to cause behavior change, including smoking cessation, the notion of self-efficacy as a reflection of recent smoking behavior change in these studies warrants greater attention in clinical research on smoking cessation treatment. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
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  • Effects of varenicline and bupropion on cognitive processes among nicotine-deprived smokers.
    Nicotine deprivation is associated with craving, negative affect, and difficulty concentrating, which may contribute to subsequent relapse. Bupropion and varenicline are both effective treatments for smoking cessation, and evidence from clinical trials suggests that these treatments increase abstinence rates. However, the mechanism by which these medications reduce relapse remains unclear. Recent research has focused on cognitive processes, such as attention and working memory, which may predict relapse. In addition, there may also be sex differences in cognitive-related deficits during nicotine deprivation. The current sample consisted of 58 (22 females) daily smokers (at least 10 cigarettes per day) randomized to receive bupropion (300 mg/day), varenicline (2 mg/day), or placebo. After a 1-week run-up phase, participants completed a 9.5-hr laboratory session after overnight abstinence (CO verified). Participants completed measures of attention (Conners' Continuous Performance Task [CPT]), working memory (digits backward), and delay discounting. Measures of craving, withdrawal, and mood were also collected. Between-subjects ANCOVA models revealed that varenicline speeded reaction time, but reduced accuracy on the CPT compared with placebo. Sex moderated the effect of bupropion compared with placebo on working memory and delay discounting. Bupropion enhanced working memory for females but not males, and this pattern was reversed for delay discounting. The current data highlight the complex processes associated with nicotine deprivation and the need for future research to examine whether cognitive-related deficits are related to relapse. Identifying these mechanisms may help in the development of new pharmacological treatments. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
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  • Effects of acute nicotine administration on resting EEG in nonsmokers.
    Smoking/nicotine has been shown to increase brain arousal states, yet previous studies have failed to distinguish between absolute improvements due to nicotine versus relief from withdrawal symptoms in smokers. This study examined the electrocortical response to nicotine in a nonsmoking population, in order to negate potential withdrawal symptoms. Twenty right-handed, nonsmoking participants were administered nicotine (6 mg) or placebo gum within a double-blind, repeated-measures design. In each session, EEG was recorded during a 2-min, resting, eyes-open condition. Nicotine administration (vs. placebo) resulted in significantly greater frontal (specifically left-frontal) alpha₂ power. Similar to previous findings in smokers. The absence of slow-wave changes following nicotine in nonsmokers suggest that these previous results in smokers may be related to withdrawal state. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
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