Database Ovid MEDLINE(R) In-Process & Other Non-Indexed Citations and Ovid MEDLINE(R) s1

NICOTINE (A) 2009 <599>

Database Ovid MEDLINE(R) In-Process & Other Non-Indexed Citations and Ovid MEDLINE(R)

Unique Identifier 19366487

Status In-Process

Authors Clemens KJ. Caille S. Stinus L. Cador M.

Authors Full Name Clemens, Kelly J. Caille, Stephanie. Stinus, Luis. Cador, Martine.

Institution

CNRS UMR 5227, Team Neuropsychopharmacology of Addiction, University of Bordeaux 1 and 2, Bordeaux, France.

Title

The addition of five minor tobacco alkaloids increases nicotine-induced hyperactivity, sensitization and intravenous self-administration in rats.

Source

International Journal of Neuropsychopharmacology. 12(10):1355-66, 2009 Nov.

Journal Name

International Journal of Neuropsychopharmacology

Country of Publication

England

Abstract

Several minor tobacco alkaloids have been found to exhibit properties pharmacologically relevant to the addictive profile of tobacco; however, little is known of their effects on a behavioural model of drug addiction. In this study we compared the locomotor and reinforcing effects of intravenous nicotine (30 microg/kg per infusion) vs. a cocktail of nicotine plus five minor alkaloids found in tobacco smoke (anabasine, nornicotine, anatabine, cotinine and myosmine). Rats were initially tested for their locomotor response to nicotine or nicotine plus the minor alkaloids with six intravenous injections over 1 h. We then assessed the spontaneous acquisition of intravenous self-administration with nicotine or nicotine plus the minor alkaloids, under a fixed-ratio 1 schedule followed by responding on a fixed-ratio 5 schedule, progressive-ratio schedule and a single within-session ascending dose-response test. The activity test was repeated following the progressive-ratio phase to assess locomotor sensitization. A second group of rats were then tested on the locomotor procedure to better clarify the role of each individual minor alkaloid in nicotine-induced locomotor activity. Compared to nicotine alone, addition of the minor tobacco alkaloids increased locomotor activity and increased locomotor sensitization following self-administration. During fixed-ratio 5, progressive ratio and the dose-response test, rats receiving nicotine plus the minor alkaloids responded significantly more than those receiving nicotine alone. Testing of each minor alkaloid in the second experiment indicated that anatabine, cotinine and myosmine individually increased nicotine-induced locomotor activity. These results suggest that the minor tobacco alkaloids, particularly anatabine, cotinine and myosmine, may increase the motivation for nicotine and thus facilitate smoking behaviour.

Publication Type Journal Article. Research Support, Non-U.S. Gov't.

Date of Publication 2009 Nov

Year of Publication 2009

Issue/Part 10

Volume 12

Page 1355-66

NICOTINE 2009 <603>

Database Ovid MEDLINE(R) In-Process & Other Non-Indexed Citations and Ovid MEDLINE(R)

Unique Identifier 19393039

Status In-Data-Review

Authors Gehricke JG. Potkin SG. Leslie FM. Loughlin SE. Whalen CK. Jamner LD. Mbogori J. Fallon JH.

Authors Full Name Gehricke, Jean-G. Potkin, Steven G. Leslie, Frances M. Loughlin, Sandra E. Whalen, Carol K. Jamner, Larry D. Mbogori, James. Fallon, James H.

Institution

Department of Psychiatry and Human Behavior, University of California, Irvine, 19722 MacArthur Blvd,, Irvine, California 92612, USA. .

Title

Nicotine-induced brain metabolism associated with anger provocation.

Source

Behavioral & Brain Functions [Electronic Resource]: BBF. 5:19, 2009.

Journal Name

Behavioral & Brain Functions [Electronic Resource]: BBF

Other ID

Source: NLM. PMC2680866

Country of Publication

England

Abstract

ABSTRACT: Cortico-limbic brain activity associated with anger may be susceptible to nicotine and, thus, may contribute to smoking initiation and nicotine addiction. The purpose of the study was to identify the brain regions that are most reactive to nicotine and show the greatest association with anger task performance. Twenty adult nonsmokers (9 women, 11 men) participated in two laboratory sessions to assess brain metabolism with fluoro deoxy-glucose Positron Emission Topography (FDG-PET) in response to nicotine and placebo patches during an anger provocation task. Outcome variables for the anger provocation task were reaction time, intensity and length of retaliation. Reaction time was associated with nicotine-induced changes in the left thalamus. Length of retaliation was associated with a functionally linked set of cortical and subcortical structures such as right frontal lobe, right anterior cingulate (BA 24), right uncus, left parietal lobe, left BA 11, left cingulate, left BA 25, left amygdala, left BA 30, left BA 38 and BA 9. These findings reveal the underlying brain circuitry targeted by nicotine during anger provocation.

Publication Type Journal Article.

Date of Publication 2009

Year of Publication 2009

Volume 5

Page 19

NICOTINE <665>

Database Ovid MEDLINE(R) In-Process & Other Non-Indexed Citations and Ovid MEDLINE(R)

Unique Identifier 19811387

Status MEDLINE

Authors West R.

Authors Full Name West, Robert.

Institution

Health Behaviour Research Centre, Department of Epidemiology and Public Health, University College London, London, England, UK.

Title

The multiple facets of cigarette addiction and what they mean for encouraging and helping smokers to stop. [Review] [42 refs]

Source

Copd: Journal of Chronic Obstructive Pulmonary Disease. 6(4):277-83, 2009 Aug.

Journal Name

Copd: Journal of Chronic Obstructive Pulmonary Disease

Country of Publication

England

Abstract

Addiction involves powerful motivation to engage in an activity repeatedly to an extent that is harmful often accompanied by impaired capacity for self-control. To effectively combat addiction to cigarettes requires an understanding that there are several mechanisms underlying it. The PRIME Theory of motivation aims to provide a model that can encapsulate these mechanisms. It recognises that evolution has led to multiple levels of motivation from basic impulses and inhibitions, through 'motives' (feelings of want and need), to 'evaluations' (beliefs about what is good or bad), and plans (intentions regarding future actions). Self-control involves self-consciously generating motives from evaluations or plans; it requires and depletes mental energy. Nicotine from cigarettes generates the motivation to smoke and undermines self-control by interacting with all of the level of motivation. It: creates stimulus-impulse associations resulting in cue-driven urges; impairs inhibitory control; gives enjoyment resulting in 'wanting' to smoke; it leads to 'nicotine hunger', withdrawal symptoms and beliefs about benefits of smoking (e.g. stress relief) all of which can result in a 'need' to smoke. Evidence is emerging that wanting to smoke (because of enjoyment) is a major deterrent to making quit attempts but does not influence success, while cue-driven impulses to smoke, nicotine hunger and adverse mood and beliefs about the benefits of smoking are important in relapse. Combating cigarette addiction requires attention to all of these factors. [References: 42]

Publication Type Journal Article. Research Support, Non-U.S. Gov't. Review.

Date of Publication 2009 Aug

Year of Publication 2009

Issue/Part 4

Volume 6

Page 277-83

NICOTINE 2009 <677>

Database Ovid MEDLINE(R) In-Process & Other Non-Indexed Citations and Ovid MEDLINE(R)

Unique Identifier 19540212

Status MEDLINE

Authors Govind AP. Vezina P. Green WN.

Authors Full Name Govind, Anitha P. Vezina, Paul. Green, William N.

Institution

Department of Neurobiology, University of Chicago, Abbot Hall 402-MC0926, Chicago, IL 60637, USA.

Title

Nicotine-induced upregulation of nicotinic receptors: underlying mechanisms and relevance to nicotine addiction. [Review] [153 refs]

Source

Biochemical Pharmacology. 78(7):756-65, 2009 Oct 1.

Journal Name

Biochemical Pharmacology

Other ID

Source: NLM. NIHMS125380 [Available on 10/01/10]

Source: NLM. PMC2728164 [Available on 10/01/10]

Country of Publication

England

Abstract

A major hurdle in defining the molecular biology of nicotine addiction has been characterizing the different nicotinic acetylcholine receptor (nAChR) subtypes in the brain and how nicotine alters their function. Mounting evidence suggests that the addictive effects of nicotine, like other drugs of abuse, occur through interactions with its receptors in the mesolimbic dopamine system, particularly ventral tegmental area (VTA) neurons, where nicotinic receptors act to modulate the release of dopamine. The molecular identity of the nicotinic receptors responsible for drug seeking behavior, their cellular and subcellular location and the mechanisms by which these receptors initiate and maintain addiction are poorly defined. In this commentary, we review how nicotinic acetylcholine receptors (nAChRs) are upregulated by nicotine exposure, the potential posttranslational events that appear to cause it and how upregulation is linked to nicotine addiction. [References: 153]

Publication Type Journal Article. Research Support, N.I.H., Extramural. Research Support, Non-U.S. Gov't. Review.

Date of Publication 2009 Oct 1

Year of Publication 2009

Issue/Part 7

Volume 78

Page 756-65

NICOTINE <678>

Database Ovid MEDLINE(R) In-Process & Other Non-Indexed Citations and Ovid MEDLINE(R)

Unique Identifier 19523455

Status MEDLINE

Authors Dwoskin LP. Smith AM. Wooters TE. Zhang Z. Crooks PA. Bardo MT.

Authors Full Name Dwoskin, Linda P. Smith, Andrew M. Wooters, Thomas E. Zhang, Zhenfa. Crooks, Peter A. Bardo, Michael T.

Institution

Department of Pharmaceutical Sciences, College of Pharmacy, University of Kentucky, Lexington, KY 40536, USA.

Title

Nicotinic receptor-based therapeutics and candidates for smoking cessation. [Review] [235 refs]

Source

Biochemical Pharmacology. 78(7):732-43, 2009 Oct 1.

Journal Name

Biochemical Pharmacology

Country of Publication

England

Abstract

Tobacco dependence is the most preventable cause of death and is a chronic, relapsing disorder in which compulsive tobacco use persists despite known negative health consequences. All currently available cessation agents (nicotine, varenicline and bupropion) have limited efficacy and are associated with high relapse rates, revealing a need for more efficacious, alternative pharmacotherapies. The major alkaloid in tobacco, nicotine, activates nicotinic receptors (nAChRs) which increase brain extracellular dopamine producing nicotine reward leading to addiction. nAChRs are located primarily presynaptically and modulate synaptic activity by regulating neurotransmitter release. Subtype-selective nAChR antagonists that block reward-relevant mesocorticolimbic and nigrostriatal dopamine release induced by nicotine may offer advantages over current therapies. An innovative approach is to provide pharmacotherapies which are antagonists at nAChR subtypes mediating nicotine evoked dopamine release. In addition, providing multiple medications with a wider array of targets and mechanisms should provide more treatment options for individuals who are not responsive to the currently available pharmacotherapies. This review summarizes the currently available smoking cessation therapies and discusses emerging potential therapeutic approaches employing pharmacological agents which act as antagonists at nicotinic receptors. [References: 235]

Publication Type Journal Article. Research Support, N.I.H., Extramural. Review.

Date of Publication 2009 Oct 1

Year of Publication 2009

Issue/Part 7

Volume 78

Page 732-43

NICOTINE 2009 <672>

Database Ovid MEDLINE(R) In-Process & Other Non-Indexed Citations and Ovid MEDLINE(R)

Unique Identifier 19728886

Status MEDLINE

Authors Fu M. Fernandez E. Martinez-Sanchez JM. Pascual JA. Schiaffino A. Agudo A. Ariza C. Borras JM. Samet JM. DCOT Study investigators.

Authors Full Name Fu, Marcela. Fernandez, Esteve. Martinez-Sanchez, Jose M. Pascual, Jose A. Schiaffino, Anna. Agudo, Antoni. Ariza, Carles. Borras, Josep M. Samet, Jonathan M. DCOT Study investigators.

Institution

Tobacco Control & Research Unit, Institut Catala d'Oncologia (ICO-IDIBELL), Av. Gran Via de L'Hospitalet 199-203, 08907 L'Hospitalet de Llobregat (Barcelona), Spain.

Title

Salivary cotinine concentrations in daily smokers in Barcelona, Spain: a cross-sectional study.

Source

BMC Public Health. 9:320, 2009.

Journal Name

BMC Public Health

Other ID

Source: NLM. PMC2749042

Country of Publication

England

Abstract

BACKGROUND: Characterizing and comparing the determinant of cotinine concentrations in different populations should facilitate a better understanding of smoking patterns and addiction. This study describes and characterizes determinants of salivary cotinine concentration in a sample of Spanish adult daily smoker men and women. METHODS: A cross-sectional study was carried out between March 2004 and December 2005 in a representative sample of 1245 people from the general population of Barcelona, Spain. A standard questionnaire was used to gather information on active tobacco smoking and passive exposure, and a saliva specimen was obtained to determine salivary cotinine concentration. Two hundred and eleven adult smokers (>16 years old) with complete data were included in the analysis. Determinants of cotinine concentrations were assessed using linear regression models. RESULTS: Salivary cotinine concentration was associated with the reported number of cigarettes smoked in the previous 24 hours (R2 = 0.339; p < 0.05). The inclusion of a quadratic component for number of cigarettes smoked in the regression analyses resulted in an improvement of the fit (R2 = 0.386; p < 0.05). Cotinine concentration differed significantly by sex, with men having higher levels. CONCLUSION: This study shows that salivary cotinine concentration is significantly associated with the number of cigarettes smoked and sex, but not with other smoking-related variables.

Publication Type Journal Article. Research Support, Non-U.S. Gov't.

Date of Publication 2009

Year of Publication 2009

Volume 9

Page 320

NICOTINE (A) <679>

Database Ovid MEDLINE(R) In-Process & Other Non-Indexed Citations and Ovid MEDLINE(R)

Unique Identifier 19501054

Status MEDLINE

Authors Rollema H. Hajos M. Seymour PA. Kozak R. Majchrzak MJ. Guanowsky V. Horner WE. Chapin DS. Hoffmann WE. Johnson DE. McLean S. Freeman J. Williams KE.

Authors Full Name Rollema, Hans. Hajos, Mihaly. Seymour, Patricia A. Kozak, Rouba. Majchrzak, Mark J. Guanowsky, Victor. Horner, Weldon E. Chapin, Doug S. Hoffmann, William E. Johnson, David E. McLean, Stafford. Freeman, Jody. Williams, Kathryn E.

Institution

Department of Neuroscience Biology, Pfizer Global Research and Development, Groton, CT 06340, USA.

Title

Preclinical pharmacology of the alpha4beta2 nAChR partial agonist varenicline related to effects on reward, mood and cognition.

Source

Biochemical Pharmacology. 78(7):813-24, 2009 Oct 1.

Journal Name

Biochemical Pharmacology

Country of Publication

England

Abstract

The pharmacological properties and pharmacokinetic profile of the alpha4beta2 nicotinic acetylcholine receptor (nAChR) partial agonist varenicline provide an advantageous combination of free brain levels and functional potencies at the target receptor that for a large part explain its efficacy as a smoking cessation aid. Since alpha4beta2 and other nAChR subtypes play important roles in mediating central processes that control reward, mood, cognition and attention, there is interest in examining the effects of selective nAChR ligands such as varenicline in preclinical animal models that assess these behaviors. Here we describe results from studies on varenicline's effects in animal models of addiction, depression, cognition and attention and discuss these in the context of recently published preclinical and preliminary clinical studies that collected data on varenicline's effects on mood, cognition and alcohol abuse disorder. Taken together, the preclinical and the limited clinical data show beneficial effects of varenicline, but further clinical studies are needed to evaluate whether the preclinical effects observed in animal models are translatable to the clinic.

Publication Type Journal Article.

Date of Publication 2009 Oct 1