Meta-analysis of the acute effects of nicotine and smoking on human performance. Psychopharmacology

Nicotine Psychopharmacology Section, National Institute on Drug Abuse, NIH Intramural Research Program, 251 Bayview Blvd., Baltimore, MD 21224, USA.
Psychopharmacology (Impact Factor: 3.88). 04/2010; 210(4):453-69. DOI: 10.1007/s00213-010-1848-1
Source: PubMed


Empirical studies indicate that nicotine enhances some aspects of attention and cognition, suggesting a role in the maintenance of tobacco dependence. The purpose of this review was to update the literature since our previous review (Heishman et al. Exp Clin Psychopharmacol 2:345-395, 1994) and to determine which aspects of human performance were most sensitive to the effects of nicotine and smoking.
We conducted a meta-analysis on the outcome measures of 41 double-blind, placebo-controlled laboratory studies published from 1994 to 2008. In all studies, nicotine was administered, and performance was assessed in healthy adult nonsmokers or smokers who were not tobacco-deprived or minimally deprived (<or=2 h).
There were sufficient effect size data to conduct meta-analyses on nine performance domains, including motor abilities, alerting and orienting attention, and episodic and working memory. We found significant positive effects of nicotine or smoking on six domains: fine motor, alerting attention-accuracy and response time (RT), orienting attention-RT, short-term episodic memory-accuracy, and working memory-RT (effect size range = 0.16 to 0.44).
The significant effects of nicotine on motor abilities, attention, and memory likely represent true performance enhancement because they are not confounded by withdrawal relief. The beneficial cognitive effects of nicotine have implications for initiation of smoking and maintenance of tobacco dependence.

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    • "The cognitive enhancement properties of nicotinic acetylcholinergic receptor (nAChR) agonists such as nicotine (Heishman et al. 2010) are associated with their moderating effects on the dopamine (DA) pathway connecting the ventral tegmental area (VTA) with cortical regions, including the prefrontal cortex (PFC). Agonists effect this enhancement by binding to nAChRs on VTA DA projection neurons, increasing dopamine signaling and processing in cortical networks (Jasinska et al. 2013; Livingstone & Wonnacott 2009; Mansvelder et al. 2006). "
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    ABSTRACT: Performance improvements in cognitive tasks requiring executive functions are evident with nicotinic acetylcholine receptor (nAChR) agonists and activation of the underlying neural circuitry supporting these cognitive effects is thought to involve dopamine neurotransmission. As individual difference in response to nicotine may be related to a functional polymorphism in the gene encoding catechol-O-methyltransferase (COMT), an enzyme that strongly influences cortical dopamine metabolism, this study examined the modulatory effects of the COMT Val158Met polymorphism on the neural response to acute nicotine as measured with resting state electroencephalographic (EEG) oscillations. In a sample of 62 healthy nonsmoking adult males, a single dose (6 mg) of nicotine gum administered in a randomized, double-blind, placebo controlled design was shown to affect α oscillatory activity, increasing power of upper α oscillations in fronto-central regions of Met/Met homozygotes and in parietal/occipital regions of Val/Met heterozygotes. Peak α frequency was also found to be faster with nicotine (vs. placebo) treatment in Val/Met heterozygotes, who exhibited a slower α frequency compared to Val/Val homozygotes. The data tentatively suggest that interindividual differences in brain α oscillations and their response to nicotinic agonist treatment are influenced by genetic mechanisms involving COMT. This article is protected by copyright. All rights reserved.
    Genes Brain and Behavior 06/2015; 14(6). DOI:10.1111/gbb.12226 · 3.66 Impact Factor
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    • "Finally, nicotine has a well-recognised positive impact upon attentional processing and a range of cognitive tasks (Leiser et al., 2009), and this has been shown in animal models, healthy volunteers, and those with schizophrenia (Heishman et al., 2010). Nicotine acts as an agonist at nAChRs, though its interactions are different to ACh: nAChRs with α4 subunits display approximately a 100-fold greater affinity for nicotine than the α7 nAChR, and unbound concentrations of nicotine achieved by smoking are too low to either inhibit or desensitise the α7 nAChR. "
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    ABSTRACT: Most individuals with schizophrenia suffer some cognitive dysfunction: such deficits are predictive of longer-term functioning; and current dopamine-blocking antipsychotics have made little impact on this domain. There is a pressing need to develop novel pharmacological agents to tackle this insidious but most disabling of problems. The acetylcholinergic system is involved in cognitive and attentional processing, and its metabotropic and nicotinic receptors are widespread throughout the brain. Deficits in acetylcholinergic functioning occur in schizophrenia, and high rates of tobacco smoking have been posited to represent a form of self-medication. The nicotinic acetylcholine receptor (nAChR) has emerged as a putative target to improve cognitive deficits in schizophrenia, and this study systematically reviewed the emerging data. Nineteen studies were identified, covering three compound classes: agonists at the α7 and α 4β2 nAChRs, and positive allosteric modulators. Overall data are underwhelming: some studies showed significant improvements in cognition but as many studies had negative findings. It remains unclear if this represents drug limitations or nascent study methodology problems. The literature is particularly hindered by variability in inclusion of smokers, generally small sample sizes, and a lack of consensus on cognitive test batteries. Future work should evaluate longer-term outcomes, and, particularly, the effects of concomitant cognitive training. © The Author(s) 2015.
    Journal of Psychopharmacology 01/2015; 29(2). DOI:10.1177/0269881114564096 · 3.59 Impact Factor
    • "Specifically, cannabis users show memory impairments that are related to cannabis use severity, resolve after 28 days of abstinence , and may be most pronounced when cannabis use is initiated during adolescence (Hanson et al., 2010; Medina et al., 2007; Pope, Gruber, Hudson, Huestis, & Yurgelun-Todd, 2001), although some evidence indicates other domains may not recover after adolescent cannabis use (Meier et al., 2012). In contrast, anecdotal (Wesnes & Warburton, 1983) and experimental data (Heishman et al., 2010; West & Hack, 1991) suggest that acute tobacco use results in improvements in concentration and memory. "
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    ABSTRACT: Objective: Co-occurring cannabis and tobacco use has become increasingly prevalent among young adults, but it is not clear how tobacco use may alter the neurocognitive profile typically observed among cannabis users. Although there is substantial evidence citing cannabis and tobacco's individual effect on episodic memory and related brain structures, few studies have examined the effect of combined cannabis and tobacco use on memory. Method: This investigation examined relationships between amount of past year cannabis and tobacco use on 4 different indices of episodic memory among a sample of young adults who identified cannabis as their drug of choice. Results: Results indicated that more cannabis use was linked with poorer initial acquisition, total learning, and delayed recall on the Hopkins Verbal Learning Test-Revised, but only among cannabis users who sporadically smoked cigarettes in the past year. Conversely, the amount of past year cannabis use was not associated with episodic memory performance among individuals who more consistently smoked cigarettes in the past year. These differences could not be explained by several relevant potential confounds. Conclusions: These findings provide important insight into a potential mechanism (i.e., attenuation of cognitive decrements) that might reinforce use of both substances and hamper cessation attempts among cannabis users who also smoke cigarettes. Ongoing and future research will help to better understand how co-use of cannabis and tobacco affects memory during acute intoxication and abstinence and the stability of these associations over time. (PsycINFO Database Record
    Neuropsychology 01/2015; 29(5). DOI:10.1037/neu0000173 · 3.27 Impact Factor
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