Article

Magnetic Resonance Imaging Studies of Cigarette Smoking

Department of Psychiatry and Biobehavioral Sciences, University of California, Los Angeles, CA, USA.
Handbook of experimental pharmacology 02/2009; 192(192):113-43. DOI: 10.1007/978-3-540-69248-5_5
Source: PubMed

ABSTRACT

This chapter reviews studies that have applied magnetic resonance imaging (MRI) toward a better understanding of the neurobiological correlates and consequences of cigarette smoking and nicotine dependence. The findings demonstrate that smokers differ from nonsmokers in regional brain structure and neurochemistry, as well as in activation in response to smoking-related stimuli and during the execution of cognitive tasks. We also review functional neuroimaging studies on the effects of nicotine administration on brain activity, both at rest and during the execution of cognitive tasks, independent of issues related to nicotine withdrawal and craving. Although chronic cigarette smoking is associated with poor cognitive performance, acute nicotine administration appears to enhance cognitive performance and increase neural efficiency in smokers.

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    • "It is now apparent that cigarette smoking-related morbidity extends well beyond cardiovascular disease, chronic obstructive pulmonary diseases, and various cancers, and includes neurobiological and neurocognitive abnormalities, some of which are progressive over time, and are not directly attributable to the foregoing biomedical conditions (Azizian et al., 2009; Durazzo et al., 2010; Sharma and Brody, 2009; Swan and Lessov-Schlaggar, 2007). "
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    ABSTRACT: Background Cigarette smoking in adults is associated with abnormalities in brain neurobiology. Smoking-induced central nervous system oxidative stress (OxS) is a potential mechanism associated with these abnormalities. The goal of this study was to compare cognitively-normal elders on cerebrospinal fluid (CSF) levels of F2-isoprostane biomarkers of OxS. Methods Elders with a lifetime history of smoking (smokers; n = 50; 75 ± 5 years of age; 34 ± 28 pack-years; approximately 12% were actively smoking at the time of study) were compared to never-smokers (n = 61; 76 ± 6 years of age) on CSF iPF2α-III and 8,12, iso-iPF2α-VI F2-isoprostanes levels. F2-isoprostanes levels were quantitated with HPLC-atmospheric pressure chemical ionization-tandem mass spectrometry. Associations between F2-isoprostanes levels, hippocampal volumes, and cigarette exposure measures were also evaluated. Results Smokers showed higher iPF2α-III level than never-smokers. An age x smoking status interaction was observed for 8,12, iso-iPF2α-VI, where smokers demonstrate a significantly greater concentration with increasing age than non-smokers. In smokers only, higher 8,12, iso-iPF2α-VI concentration was associated with smaller hippocampal volume, and greater iPF2α-III level was related to greater pack years. Conclusions This is the first study to demonstrate that a history of cigarette smoking in cognitively-normal elders was associated with significantly elevated CSF F2-isoprostane levels and greater age-related increases in F2-isoprostane levels, and that higher F2-isoprostane levels in smokers were related to smaller hippocampal volume. These findings provide additional novel evidence that a history of chronic smoking during adulthood is associated with adverse effects on the human brain that are potentially persistent even with extended smoking cessation.
    Full-text · Article · Sep 2014 · Drug and Alcohol Dependence
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    • "Active-smokers showed significantly higher cortical F 4 -neuroprostane level, a measure of free radical-mediated lipid peroxidation in neurons. Thus, the persistently elevated level of OxS imposed by chronic cigarette smoking may serve as a primary mechanism contributing to the hippocampal volume deficits observed in this study, as well as the other neurobiological and neurocognitive abnormalities observed in clinical and non-clinical cohorts of chronic smokers across the lifespan (for review, see Azizian et al., 2009; Durazzo et al., 2010). See (Durazzo et al., 2010) for a more detailed discussion on OxS and other potential mechanisms contributing to neurobiological and neurocognitive dysfunction in chronic smokers. "
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    ABSTRACT: Previous cross-sectional MRI studies with healthy, young-to-middle-aged adults reported no significant differences between smokers and non-smokers on total hippocampal volume. However, these studies did not specifically test for greater age-related volume loss in the total hippocampus or hippocampal subregions in smokers, and did they did not examine relationships between hippocampal and subfield volumes and episodic learning and memory performance. Healthy, young-to-middle-aged (45±12 years of age) smokers (n=39) and non-smokers (n=43) were compared on total hippocampal and subfield volumes derived from high-resolution 4Tesla MRI, emphasizing testing for greater age-related volume losses in smokers. Associations between hippocampal volumes and measures of episodic learning and memory were examined. Smokers showed significantly smaller volumes, as well as greater volume loss with increasing age than non-smokers in the bilateral total hippocampus and multiple subfields. In smokers, greater pack-years were associated with smaller volumes of the total hippocampus, presubiculum, and subiculum. In the entire cohort, performance on measures of learning and memory was related to larger total hippocampal and several subfield volumes, predominately in the left hemisphere. Chronic cigarette smoking in this young-to-middle aged cohort was associated with smaller total hippocampal and subfield volumes, which were exacerbated by advancing age. Findings also indicated an adverse smoking dose/duration response (i.e., pack-years) with total hippocampal and select subfield volumes. These hippocampal volume abnormalities in smokers may be related to the deficiencies in episodic learning and memory in young-to-middle-aged smokers reported in previous studies.
    Full-text · Article · Sep 2013 · Drug and alcohol dependence
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    • "While the rewarding properties of nicotine have been extensively studied (Corrigall et al, 1992Corrigall et al, , 1994 Grieder et al, 2012; Laviolette et al, 2008; Laviolette and van der Kooy, 2003), the neural substrates associated with withdrawal are not as well characterized. Activation of diverse brain regions has been correlated with cognitive withdrawal symptoms and craving (Azizian et al, 2009; Davis and Gould, 2009; McClernon and Gilbert, 2004). Although craving and cognitive impairments are reliable markers of nicotine withdrawal (Kenney and Gould, 2008; Levin et al, 2006; McClernon et al, 2004; Rezvani and Levin, 2001), anxiety has been shown to impact relapse rate as well (Dani and Harris, 2005; DiMatteo et al, 2000). "
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    ABSTRACT: Smoking is the largest preventable cause of death in the United States. Furthermore, a recent study found that <10% of quit attempts resulted in continuous abstinence for 1 year. With the introduction of pharmacotherapies like Chantix (varenicline), a selective α4β2 nicotinic partial agonist, successful quit attempts have significantly increased. Therefore, novel subtype-specific nicotinic drugs, such as sazetidine-A, present a rich area for investigation of therapeutic potential in smoking cessation. The present studies examine the anxiety-related behavioral and functional effects of the nicotinic partial agonists varenicline and sazetidine-A during withdrawal from chronic nicotine in mice. Our studies indicate that ventral hippocampal-specific infusions of sazetidine-A, but not varenicline, are efficacious in reducing nicotine withdrawal-related anxiety-like phenotypes in the novelty-induced hypophagia (NIH) paradigm. To further investigate functional differences between these partial agonists, we utilized voltage-sensitive dye imaging (VSDi) in ventral hippocampal slices to determine the effects of sazetidine-A and varenicline in animals chronically treated with saline, nicotine, or undergoing 24 h withdrawal. These studies demonstrate a functional dissociation of varenicline and sazetidine-A on hippocampal network activity, which is directly related to previous drug exposure. Furthermore, the effects of the nicotinic partial agonists in VSDi assays are significantly correlated with their behavioral effects in the NIH test. These findings highlight the importance of drug history in understanding the mechanisms through which nicotinic compounds may be aiding smoking cessation in individuals experiencing withdrawal-associated anxiety.
    Full-text · Article · Apr 2013 · Neuropsychopharmacology: official publication of the American College of Neuropsychopharmacology
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