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Nicotine psychopharmacology in man
Abstract
The present within-subjects, crossover study was designed to assess the short-term effects of several nicotine replacement strategies. After completing a 2 day smoking baseline, 18 (7 M, 11 F) smokers(≥ 20 cpd) went through the following conditions, each for two full days, in randomized order: a)nicotine chewing gum; b) 24 hour nicotine patch; c) 16 hour nicotine patch; d) two 24 hour nicotine patches; e) 24 hour nicotine patch plus nicotine gum; f) no medication. Only conditions b, c, d, and f will be compared here. Subjects provided self-report and objective data on 5 occasions during each 2 day period (7–8 AM &5–6 PM), and smoked ad lib for the 5 days between conditions. Between group comparisons of abnormal dreams found (at AM visit): 24 hour patch double & 24 hour patch > baseline. Between group comparisons of interrupted sleep found (at AM visit): double 24 hour patch > baseline. Between group comparisons of difficulty getting to sleep found (at AM visit): double 24 hour patch > baseline & 16 hour patch. Saliva nicotine and cotinine values will be presented. These results suggest that use of a double strength nicotine patch can have significant effects on sleep. While some subjects on 24 hour patch reported sleep disturbances, there was no significant difference between 16 & 24 patch use on self-reported sleep disturbances.
... Several studies have documented how addiction among nurses threatens professional standards and the delivery of quality care to patients (Padula, 1992;Trinkoff & Storr, 1998). Addiction is a complex and multidimensional process that involves biological, psychological, and social factors (Henningfield, Cohen, & Pickworth, 1994). The term addiction is often equated with abuse and/or dependence. ...
... Landmark reports about the addictive properties of nicotine Henningfield et al., 1994; Caught in the Middle: Experiences of Tobacco-Dependent Nurse Practitioners ...
To explore how tobacco-dependent nurse practitioners (NPs) describe their experiences with health promotion and disease prevention practices with patients who smoke.
Twelve NPs who completed a graduate level NP program of study participated in face-to-face interviews and/or online chat room interviews.
Participants' responses revealed three themes relevant to their experience as tobacco-dependent clinicians with health promotion responsibilities. These themes centered around (a) living as an insider in the world of tobacco addiction, (b) having the outside-in view of living with a tobacco addiction, and (c) being caught in the middle of a tobacco addiction.
All of the tobacco-dependent participants described limited smoking-cessation interventions with their patients. A barrier to implementation of more aggressive interventions, perhaps, is the provider's own tobacco addiction. With increasing evidence that tobacco-dependent health care professionals are not adequately intervening with tobacco-dependent patients, effective strategies are needed to assist and/or support not only tobacco-dependent patients but providers as well.
... 4 Nicotine in cigarettes modulates stress temporarily. 5 Religious beliefs are among the factors that can be effective in preventing and reducing mental disorders, as well as reducing problems, such as suicide, addiction, depression, stress, and anxiety. 6 Religious beliefs lead to improved health and quality of life (QOL), and increased selfesteem. ...
Background:
Psychological stress is associated with unhealthy lifestyles, including smoking. Moreover, religious beliefs can play a significant role in relieving mental disorders such as anxiety and stress. Due to the frequent exposure of medical students to stressful situations, this study was conducted with the aim to investigate the relationship of internal and external religious orientation with perceived stress and nicotine dependence.
Methods:
This correlational study was carried out on medical students of Kerman University of Medical Sciences, Kerman, Iran, in 2015. The sample size was determined to be 224 individuals using the Morgan table. The participants were selected using stratified random ýsampling. The data collection tools consisted of a demographic information form, the Religious Orientation Scale (ROS) (Allport and Ross), the Perceived Stress Scale (PSS-14), and the Fagerstrom Test for Nicotine Dependence (FTND). Data were analyzed using multiple regression analysis, analysis of variance (ANOVA), Pearson correlation coefficient, and t-test in SPSS software.
Findings:
The findings of the study showed that internal religious orientation had a significant negative relationship with perceived stress and nicotine dependence; however, no significant relationship was observed between external religious orientation and these variables.
Conclusion:
Based on the results of the study, it can be concluded that the religious beliefs of individuals have a preventive role in perceived stress and nicotine dependence.
... Department of Health and Human Services, 1988). Speed and dose of nicotine's absorption in the body is controlled by tobacco's pH level and delivery method (Henningfield, Cohen, & Pickworth, 1993;Henningfield & Keenan, 1993). ...
Tobacco use continues to be the leading cause of morbidity and mortality in the United States. Public Health Service sponsored clinical guidelines support smoking cessation interventions at every clinical encounter with a smoking patient. The primary aim of this research protocol proposed to examine the efficacy of a 12-week nurse-delivered relapse management intervention designed with conceptual underpinnings from Self-efficacy Theory to enhance smoking abstinence of hospitalized smokers following their hospital discharge. A randomized, controlled two-group design with an intent-to-treat approach was used. The sample consisted of 80 consenting smokers prospectively recruited during hospitalization. Subjects were randomly assigned by equal allocation to a special intervention group (SI) or an enhanced usual only group (UC). All subjects received enhanced usual care. Participants assigned to the intervention group received 8 telephone intervention sessions with a nurse over 11 weeks after discharge. Intervention was directed towards enhancing self-efficacy to maintain tobacco abstinence. Follow-up visits occurred 12 and 24 weeks following hospital discharge. Data collection included smoking point prevalence with validation by exhaled carbon monoxide. At 12 weeks, 20% (n = 8) UC and 40% (16) SI subjects were abstinent (LRƒÓ2 = 4.87, df = 1, p = .014). At 24 weeks, 15% (n = 6) UC and 42% (n = 16) SI subjects were abstinent (LRƒÓ2 = 7.69, df = 1, p = .004). There were significant differences between treatment assignments, particularly when confounding variables for current employment and greater lengths of hospital stay were controlled in the analyses. Self-efficacy with the Relapse Situation Efficacy Questionnaire was predictive of 12-week smoking status. Treatment adherence was significantly related to smoking behavior in the treatment group. The two groups did not differ in smoking lapse or with self-efficacy over time. Recruitment sites did differ with respect to smoking status, but only at 12-weeks after discharge. There were no significant cohort differences. Future research is needed to improve tobacco abstinence following hospitalization and to examine treatment adherence with an emphasis on strategies for improvement of treatment adherence with hospitalized smokers.
... Stress seems to be consistently related to the smoking behavior and the Abuse of various other drugs (Hemmingsson et al., 2008). Smoking has found to be a coping tool in order to deal with stress as nicotine has pharmacological affects that moderates stress level (Henningfield et al., 1995;Marlatt and Cordon, 1985;Shiffman et al., 2007). In addition, once smoker has adopted smoking behavior as a strategy for coping after that they will be less willing to see the need to try to develop active and healthier strategies for coping. ...
Organizational Climate is a driving force in the organization behavior which provides foundations to many physical and psychological phenomena to the employees. Bullying is one of the major under considered phenomenon, usually caused by the organizational climate. The objective of the study is to examine the relationship between organizational climates, workplace bullying and workers’ health in selected higher education institutes of Pakistan. A proportionate random sample of 20 Universities comprising of 10 from public sector and 10 from private sector was selected for the study. The model of workplace bullying, organizational climate and worker's health was estimated by Structural Equation Modeling using AMOS software. The study found a negative relationship between organizational climate and bullying on one hand, while on the other hand, an increased workplace bullying effects employees’ health negatively due to affected sleeping hours. Drug abuse was treated as a moderator between health and affected sleeping hours. The study suggested that organizations should control workplace bullying which may cause physical and psychological effects on employee's health.
... The range of concentrations of nicotine encountered in cigarettes or smokeless tobacco can affect HPLF viability and metabolism. Cigarettes can deliver up to 1900μg nicotine per cigarette (Henningfield et al, 1993). If one smokes one pack of cigarettes per day, one can be exposed to 38,000μg of nicotine. ...
Purpose: To determine the influence of nicotine upon the release of interleukin-6 (IL-6) from human periodontal ligament fibroblasts (HPLF). Methods and Materials: The HPLF were exposed to nicotine concentrations of 125 to 1500 μg/ml for 24 hours (h). IL-6 release and cell growth were determined after exposure to the different nicotine concentrations after 24 hours. IL-6 levels were measured by enzyme-linked immunosorbent assay (ELISA). Cell counts were determined with a Coulter counter. Results: HPLF cell counts were significantly higher than untreated cells after nicotine exposure of 375 μg/ml and significant-ly lower than untreated cells for cells treated with 1500 μg/ml nicotine. After 24 h of cell exposure to nicotine concentrations of 250 and 375 μg/ml, HPLF release of IL-6 per cell was significantly higher than that of untreated HPLF. HPLF treated with 1500 μg/ml, nicotine released significantly less IL-6 per cell than did untreated cells. Conclusions: These results indicate that nicotine can increase IL-6 release from HPLF.
... Hiere seems to be tacit acceptance by many researchers that smoking has effects that are psychologically beneficial and that this is due to the fact that it is an effective method of delivering nicotine into the body. Some laboratories have consistently reported positive findings (see Warburton, 1992). Yet the evidence by no means unequivocally supports this view. ...
... Department of Health and Human Services [USDHHS], 1988), although several workers in the field had so construed it for many years (e.g., Russell, 1976). There is now scientific consensus that nicotine is addictive by any reasonable definition (Henningfield, Cohen, & Pickworth, 1993;Kaplan, Orleans, Perkins, & Pierce, 1995;USDHHS, 1988). Cigarettes, the primary vehicle for delivering nicotine, are a legal product heavily marketed by the tobacco industry. ...
There are now over 450 active Nicotine Anonymous meetings (groups) in the United States. The origins and current status of Nicotine Anonymous are described, and some comparisons are drawn with Alcoholics Anonymous. Several research issues are identified including determination of what kinds of smokers are attracted to, stick with, and benefit from Nicotine Anonymous; describing patterns of utilization; and the degree to which Nicotine Anonymous meetings follow 12-step principles and procedures. From a service perspective, Nicotine Anonymous may serve as a useful referral resource for smokers with alcohol- or substance-abuse comorbidities, especially those who have participated in 12-step programs. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
... Addiction models tend to emphasize the pharmacological properties and conditioned effects of nicotine. Nicotine is viewed both as a negative reinforcer, such that smokers smoke to maintain steady state blood nicotine levels and avoid withdrawal, and as a positive reinforcer whose effects on mood, arousal, and concentration are sought (Henningfield, Cohen, & Pickworth, 1993;Pomerleau & Pomerleau, 1984). In this model, attempts at smoking cessation are largely determined by degree of addiction and strategies to cope with the consequences of addiction, notably withdrawal. ...
Smoking cessation research and programs are shifting toward reaching populations. A framework for intervention for tobacco and other addictive behaviors is presented that can accommodate this emerging paradigm as well as more traditional clinical approaches. Smoking cessation is seen to be determined by 3 sets of factors: (a) motivation, which includes both readiness to try to quit and persistence in the face of withdrawal and stress; (b) addiction level; and (c) environmental supports and barriers. Coping skills that provide ways of dealing with these factors are seen as the essential content of cessation programs. The implications of this framework for assessment and intervention are discussed, with particular attention to the different requirements of clinical (intensive, aimed at self-selected smokers) and population-based (brief, aimed at all smokers in a setting) programs. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
... The instruction to smoke one cigarette immediately was to standardize the number of hours since the last cigarette. The literature indicates that 24 hr of abstinence is appropriate for initiating nicotine withdrawal (Henningfield, Cohen, & Pickworth, 1993). Using a semi-random procedure, half of the participants were assigned to the normal smoking condition and the other half in the abstinence condition for session 1. ...
Given the lack of consensus regarding changes in temporal and probability discounting as a function of smoking abstinence in cigarette smokers, the present study comprehensively examined possible changes in these processes following a period of acute smoking abstinence consistent with elevated withdrawal symptoms and craving.
Computerized temporal and probability discounting assessments were collected from cigarette smokers following normal smoking and 24-hr smoking abstinence, with the order of normal smoking and abstinence sessions counterbalanced across participants. Other conditions included commodity (money and cigarettes), sign (gains and losses), and magnitude ($50 and $1,000).
Twenty four-hour smoking abstinence resulted in a reduction in expired carbon monoxide to near-zero levels and increases in withdrawal and craving. Examination of discounting parameters as a function of smoking abstinence revealed a general pattern of increase in the temporal discounting of monetary gains and losses following abstinence but not in the temporal discounting of cigarettes nor probability discounting of money or cigarettes. Pearson correlations also revealed an expected pattern of significant relationships.
The present study is a comprehensive examination of temporal and probability discounting following smoking abstinence and reveals a generalized change in intertemporal decision making for monetary rewards.
... In spite of that variability in consumption, significant increases in toxin exposure after B&M and B&Mf were observed. These results confirm that cigarillos deliver quantities of nicotine that could initiate or sustain dependence and deliver CO and other toxicants to the lower respiratory tract (Henningfield, Cohen, & Pickworth, 1993), which could lead to the respiratory diseases usually associated with cigarette smoking. ...
Over the past 20 years, there has been a tripling in the consumption of small cigars and cigarillos, with further increases expected because cigar products are not subject to Food and Drug Administration regulations. Acute toxin exposure from cigar smoking is difficult to assess because unlike cigarettes, cigars vary widely in size, design, composition, and in the smoking behavior of their consumers. For example, a recent practice among urban youth is to remove the paper liner (i.e., "freaking") of a small cigar in the belief that it is this paper liner that leads to addiction and cancer.
We examined acute exposure (CO and nicotine boosts) and puffing behavior in 12 participants (10 men) who smoked (ad lib) their usual conventional cigarette, a Black & Mild cigar (B&M) and a B&M without the paper liner (i.e., "freaked" [B&Mf]).
All products (cigarettes, B&M, and B&Mf) significantly increased heart rate and CO with a trend for plasma nicotine. Nicotine boost was significantly higher after cigarette smoking than both B&M and B&Mf, while CO boost was significantly greater after B&M and B&Mf than cigarettes. The CO boost after B&M was larger than after B&Mf.
These findings suggest that small cigar smoking is associated with smoke inhalation that leads to significant exposure to nicotine, CO, and presumably other components of tobacco smoke and that removing the inner liner does not substantially reduce toxin exposure.
... Yet another explanation for why NRT has not had a more pronounced effect on influencing population trends in smoking behavior concerns the inadequacies of the current dosage strengths and formulations of nicotine medications (6,80). The reinforcing effect of nicotine depends on the amount of nicotine and the way in which nicotine enters the blood stream (5,6,27,41,80,91). Nicotine in cigarette smoke is absorbed in the lungs (91). ...
This review summarizes evidence pertaining to the role of nicotine medications in smoking cessation and focuses particularly on evaluating evidence of the impact that nicotine replacement therapies (NRT) have had on altering population trends in smoking behavior. Accumulated evidence from controlled clinical trials has demonstrated that available forms of NRT (e.g., gum, transdermal patch, nasal spray, inhaler, and lozenge) increase quit rates compared with placebos by 50%-100%. However, despite the positive results from these studies, fewer than one in five smokers making a quit attempt do so with the benefit of NRT. Because not enough smokers are using NRT, the availability of NRT has not had a measurable impact on influencing population trends in smoking behavior. Among the factors contributing to the low utilization of nicotine medications are the inadequacies of the current dosage strengths and formulations of existing medications, smokers' perceptions of the high cost of the drugs, and concerns that many smokers have about safety and efficacy of nicotine medications.
Delta and kappa opioid receptors (DOR and KOR, respectively) and their endogenous ligands, proenkephalin (PENK) and prodynorphin (PDYN)-derived opioid peptides are proposed as important mediators of nicotine reward. The present study investigated the regulatory effect of chronic nicotine treatment on the gene expression of DOR, KOR, PENK and PDYN in the mesocorticolimbic system. Three groups of rats were injected subcutaneously with nicotine at doses of 0.2, 0.4 or 0.6 mg/kg/day for six days. Rats were decapitated one hour after the last dose on day six, as this timing coincides with increased dopamine release in the mesocorticolimbic system. mRNA levels in the ventral tegmental area (VTA), lateral hypothalamic area (LHA), amygdala (AMG), dorsal striatum (DST), nucleus accumbens and medial prefrontal cortex were measured by quantitative real-time PCR. Our results showed that nicotine upregulated DOR mRNA in the VTA at all of the doses employed, in the AMG at the 0.4 and 0.6 mg/kg doses, and in the DST at the 0.4 mg/kg dose. On the other hand, PDYN mRNA was reduced in the LHA with 0.6 mg/kg nicotine and in the AMG with 0.4 mg/kg nicotine. KOR mRNA was also decreased in the DST with 0.6 mg/kg nicotine. Nicotine did not regulate PENK mRNA in any brain region studied. This article is protected by copyright. All rights reserved.
Presenilin-1 (PS1) is a core component of γ-secretase that is involved in neurodegeneration. We have previously shown that PS1 interacts with a MAPK (JNK), and another MAPK (p38) is activated by ethanol withdrawal (EW), abrupt termination from chronic ethanol-exposure. EW is excitotoxic in nature, induces glutamate upregulation, and provokes neuronal damage. Here, we explored a potential mechanistic pathway involving glutamate, p38 (p38α isozyme), and PS1 that may mediate EW-induced excitotoxic stress. We used the prefrontal cortex of male rats withdrawn from a chronic ethanol diet. Additionally, we used ethanol withdrawn HT22 cells (mouse hippocampal) treated with the inhibitor of glutamate receptors (MK-801), p38α (SB203580), or γ-secretase (DAPT) during EW. Separately, ethanol-free HT22 cells were exposed to glutamate with or without SB203580 or DAPT. Protein levels, mRNA levels, and cell viability were assessed using immunoblotting, q-PCR, and Calcein assay, respectively. The prefrontal cortex of ethanol withdrawn rats or HT22 cells showed an increase in PS1 and p38α, which was attenuated by MK-801 and SB203580, but mimicked by glutamate treatment to ethanol-free HT22 cells. DAPT attenuated the toxic effect of EW or glutamate on HT22 cells. These results suggest that PS1 expression is triggered by glutamate through p38α, contributing to the excitotoxic stimulus of EW.
Although the effect of gene-gene interaction on nicotine-dopamine metabolism for smoking behavior has been reported, polymorphisms of dopamine D2 receptor (DRD2) and monoamine oxidase A (MAOA) have not been simultaneously examined among smokers. In this study, 481 young Taiwanese men completed a self-report questionnaire on smoking status, and data were obtained on polymorphisms of DRD2 rs1800497, DRD2 rs1079597, MAOA rs309850, and MAOA rs1137070, urinary nicotine, and urinary cotinine. In a comparison of 261 current smokers and 220 never smokers, odds ratios (ORs) for the development of smoking in all genotypes were not statistically significant. Among smokers with DRD2 rs1079597 GG//MAOA rs309850 3-repeat, the OR of heavier smoking was 2.67 times higher (95% confidence interval [CI]: [1.08, 6.59], p = .031) and the score on the Fagerstrom test for nicotine dependence was higher (4.26 vs. 2.83) than in those with DRD2 rs1079597 AA//MAOA rs309850 3-repeat. Adjusted urinary cotinine concentration was significantly different between those two groups (median value: 95.83 ng/μl vs. 133.24 ng/μl, respectively, p = .045). These findings suggest that the interaction of DRD2 rs1079597 and MAOA rs309850 3-repeat affects smoking intensity in young Taiwanese men.
© The Author(s) 2015.
Tobacco use is the leading preventable cause of morbidity and death in the United States. Because 80% to 90% of adult smokers began during adolescence, and two thirds became regular, daily smokers before they reached 19 years of age, tobacco use may be viewed as a pediatric disease. Every year in the United States, approximately 1.4 million children younger than 18 years start smoking, and many of them will die prematurely from a smoking-related disease. Moreover, there is recent evidence that adolescents report symptoms of tobacco dependence early in the smoking process, even before becoming daily smokers. The prevalence of tobacco use is higher among teenagers and young adults than among older adult populations. The critical role of pediatricians in helping to reduce tobacco use and addiction and secondhand tobacco-smoke exposure in the pediatric population includes education and prevention, screening and detection, and treatment and referral.
Purpose
The purpose of this paper is to investigate whether university students' smoking behaviour is associated with higher levels of stress and depression directly, or indirectly, via the mediation of coping, personal beliefs and social support.
Design/methodology/approach
The study design involves a cross‐sectional survey. Structural equation modelling was employed to explore the relationships between smoking behaviour, stress and depression via the mediating effects of coping resources, personal beliefs and social support.
Findings
The higher the stress and depression levels, the more likely the respondents' were to adopt disengagement coping strategies and to engage in smoking behaviour. Stress was not found to have a significant direct effect on smoking behaviour when depression, active coping abilities and social support were included as mediators in the model. Thus, if stress is high yet coping skills are also high and personal beliefs are anti‐smoking, the likelihood of smoking was low.
Research limitations/implications
Disengagement coping strategies significantly increased the likelihood of smoking when stress heightened depression level. However, stress did not independently increase the chance of smoking when active coping and social support were moderating the effects of depression on smoking behaviour. Personal beliefs also acted as an independent contributor to increase the likelihood of smoking when pro‐smoking beliefs were held by individuals. Overall, this study suggests that personal coping strategies and personal beliefs, with social support, are important protective mechanisms through which stress and depression influence smoking behaviour.
Practical implications
Health promotion programmes to encourage smoking cessation should therefore include measures to encourage young adults to adopt active coping strategies (e.g. exercise, recreational activities) to make interventions effective in reducing smoking rate.
Originality/value
This study identifies important mechanisms that underpin smoking behaviour among university students. The results provide evidence that supports the resilience perspective that personal coping resources, personal beliefs and protective factors, such as social support, are important factors either to lead people to adopt smoking behaviour, or to decrease the likelihood of smoking.
This study examined plasma cotinine replacement levels of 56 outpatient smokers administered a 21 mg/day transdermal nicotine patch (Nicoderm CQ®). The percentage of cotinine replacement ranged from 35 to 232% (mean 107%; median 90.5%). Four subject variables were found to be significantly correlated with percentage of cotinine replacement-baseline cotinine level, prior quit attempts, gender, and the Fagerström Tolerance Questionnaire score. A two-variable model consisting of baseline cotinine level and gender provided the most powerful predictor combination. The percentage of cotinine replacement was not predictive of post-treatment smoking. The relatively high levels of cotinine replacement obtained using the Nicoderm CQ® 21 mg/day patch suggest cautious use of higher dose treatment with this particular patch.
Genetic variation may influence initial sensitivity to nicotine (i.e. during early tobacco exposure), perhaps helping to explain differential vulnerability to nicotine dependence. This study explored associations of functional candidate gene polymorphisms with initial sensitivity to nicotine in 101 young adult nonsmokers of European ancestry. Nicotine (0, 5, 10 microg/kg) was administered through nasal spray followed by mood, nicotine reward (e.g. 'liking') and perception (e.g. 'feel effects') measures, physiological responses, sensory processing (prepulse inhibition of startle), and performance tasks. Nicotine reinforcement was assessed in a separate session using a nicotine versus placebo spray choice procedure. For the dopamine D4 receptor [DRD4 variable number of tandem repeats (VNTR)], presence of the 7-repeat allele was associated with greater aversive responses to nicotine (decreases in 'vigor', positive affect, and rapid information processing; increased cortisol) and reduced nicotine choice. Individuals with at least one DRD4 7-repeat allele also reported increased 'feel effects' and greater startle response, but in men only. Other genetic associations were also observed in men but not women, such as greater 'feel effects' and anger, and reduced fatigue, in the dopamine D2 receptor (DRD2 C957T single nucleotide polymorphism) TT versus CT or CC genotypes. Very few or no significant associations were seen for the DRD2/ANKK1 TaqIA polymorphism, the serotonin transporter promoter VNTR or 5HTTLPR (SLC6A4), the dopamine transporter 3' VNTR (SLC6A3), and the mu opioid receptor A118G single nucleotide polymorphism (mu opioid receptor polymorphism 1). Although these results are preliminary, this study is the first to suggest that genetic polymorphisms related to function in the dopamine D4, and perhaps D2, receptor may modulate initial sensitivity to nicotine before the onset of dependence and may do so differentially between men and women.
Six specific hypotheses regarding putative mechanisms by which stressful life events might lead to initiation of smoking among adolescents were proposed and tested on a Grade 6 cohort of students in Scarborough, Ontario, Canada. In addition, the data were used to determine the set of risk factors for initiation of smoking most pertinent to the experience of the cohort.
The same relationships were examined for the 1,543 students when they were in Grade 8 and compared to the earlier Grade 6 results. The hypotheses include the effects of personal resources (coping, self-esteem, social support, and mastery), social conformity, rebelliousness, attitudes, smoking environment factors, and gender differences.
The hypotheses were not unequivocally supported, except for the hypotheses about attitudes and smoking environment as well as gender effects. Males and females differ with regard to the variables and interrelationships in both years and in the final models developed. In Grade 6, there are more smoking environment items for males than for females. By Grade 8, male smoking is influenced by mastery, social conformity, and rebelliousness, while for females environmental smoking and rebelliousness are important.
Male and female students differ in how stress, depression, and smoking are related in the presence of psychosocial factors.
The purpose of this article is to develop an understanding of people who smoke and how they change as a foundation for the delivery of smoking cessation interventions in primary care. Central to our approach is the transtheoretical model of change (TMC). The TMC is an evidence-based model of behavior change that has been developed and tested during the past 2 decades by Prochaska and his colleagues in the context of smoking cessation. We use a review of the literature, in-depth interviews of people who successfully quit smoking, and our experience applying the TMC in the context of primary care and a smoking cessation clinic to explore the clinical work of smoking cessation. This article on smoking cessation will be presented in 2 issues. Part 1 describes the theoretical information known about smoking cessation: why smoking is a powerful behavior, the scientific background of the TMC, and the building-block constructs of the TMC. The first section of part 2 is a review of the Public Health Service clinical practice guideline, Treating Tobacco Use and Dependence, published in 2000. The second section of part 2 is a discussion of clinical assessments and strategies for working with smokers, which is grounded in the Public Health Service practice guideline, our understanding of people who smoke, and the TMC. Woven throughout are transcripts of interviews with 4 people in which they describe their smoking experiences and their pathways to cessation.
Chronic ethanol abuse causes up-regulation of NMDA receptors, which underlies seizures and brain damage upon ethanol withdrawal (EW). Here we show that tissue-plasminogen activator (tPA), a protease implicated in neuronal plasticity and seizures, is induced in the limbic system by chronic ethanol consumption, temporally coinciding with up-regulation of NMDA receptors. tPA interacts with NR2B-containing NMDA receptors and is required for up-regulation of the NR2B subunit in response to ethanol. As a consequence, tPA-deficient mice have reduced NR2B, extracellular signal-regulated kinase 1/2 phosphorylation, and seizures after EW. tPA-mediated facilitation of EW seizures is abolished by NR2B-specific NMDA antagonist ifenprodil. These results indicate that tPA mediates the development of physical dependence on ethanol by regulating NR2B-containing NMDA receptors.
• proteases
• excitotoxicity
• alcoholism
The desensitization of alpha-bungarotoxin-insensitive native neuronal nicotinic receptors was studied in rat cortical cell cultures using the patch clamp technique. Thirty-minute perfusions of nicotine reduced currents evoked by short test pulses of 300 microM acetylcholine over a range of 3 to 300 nM, with an IC50 of 51 nM. The time course of desensitization onset was fit by a biexponential function consisting of a fast time constant of about 1 min and a slower component of 6-10 min. The desensitization recovery process was also biexponential and was dominated by a slow time constant of 12-20 min, as well as a minor component of about 1 min. The intracellular dialysis of either the protein kinase C activator phorbol-12-myristate-13 acetate or the phosphatase inhibitor cyclosporin A accelerated the desensitization recovery rate by 2-fold. The data imply that endogenous cortical nicotinic receptor channels may enter one of two desensitization states. The first state (D1) is characterized by rapid entry and recovery, whereas transitions into and out of the second state (D2) occur at slower rates. The D2 receptor state may arise by a sequential transition from the D1 conformation. Protein kinase C activation or phosphatase 2B inhibition may favor the D1 receptor state over that of D2 to promote faster overall rates of desensitization recovery.
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