Cigarette Smoking, Suicidal Behavior, and Serotonin Function in Major Psychiatric Disorders

Malone, Kevin; Waternaux, Christine; Haas, Gretchen L.; Cooper, Thomas B.; Li, Shuhua; Mann, J. John

doi:10.1176/appi.ajp.160.4.773

Cited by 245 publications

(194 citation statements)

References 54 publications

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“…28,29 In human studies Malone et al have reported a correlation between cigarette smoking and impaired serotonin function in depressed patients by measuring cerebrospinal fluid 5-hydroxyindoleacetic acid level and investigating prolactin response to fenfluramine. 7 Reduced serotonergic function in the brain is also suggested by studying the post-mortem brains of depressed suicide victims; they have lower brainstem levels of 5HT and 5HIAA, and fewer 5HTT binding sites in the prefrontal cortex. 12 In vivo imaging and post-mortem brain studies conducted in depressed patients suggested that reduced 5HTT binding is widespread in the brain.…”

Section: Discussionmentioning

confidence: 99%

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Chronic effect of nicotine on serotonin transporter mRNA in the raphe nucleus of rats: Reversal by co‐administration of bupropion

Semba

Wakuta

2008

Psychiatry Clin Neurosci

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Aim: Epidemiologic studies suggest the existence of a biological link between nicotine withdrawal and depression. To investigate the neuronal mechanisms of the precipitation of depression during smoking cessation, an animal model of nicotine withdrawal was used, and the expression of serotonin transporter (5HTT), abnormality of which is implicated in the pathogenesis of depression, was investigated. The effect of co-administration of bupropion, which has been clinically shown to ameliorate nicotine withdrawal symptoms, was also investigated in this model. Methods:Male Wistar rats were implanted with a minipump s.c., which delivered nicotine at a rate of 6 mg/kg per day for 12 days (days 1-12). Rats given chronic nicotine were killed on day 13, or 2 days after the removal of minipump (withdrawal day 2). In a separate experiment, bupropion (15 or 30 mg/kg per day) was injected into the nicotine infused rats on days 2-12. The expression of mRNA for 5HTT in the dorsal raphe was determined on in situ hybridization.Results: Chronic nicotine infusion resulted in the reduction of 5HTT mRNA expression, which lasted through withdrawal day 2. Co-administration of bupropion, however, significantly antagonized this reduction.Conclusions: Chronic nicotine infusion reduces the synthesis of 5HTT protein, which may consequently precipitate depression during nicotine withdrawal, but co-administration of bupropion may ameliorate withdrawal symptoms by counteracting nicotine's effect on 5HTT.

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Section: Discussionmentioning

confidence: 99%

“…Male Wistar rats were implanted with a minipump s.c., which delivered nicotine at a rate of 6 mg/kg per day for 12 days (days [1][2][3][4][5][6][7][8][9][10][11][12]. Rats given chronic nicotine were killed on day 13, or 2 days after the removal of minipump (withdrawal day 2).…”

Section: Methodsmentioning

confidence: 99%

Chronic effect of nicotine on serotonin transporter mRNA in the raphe nucleus of rats: Reversal by co‐administration of bupropion

Semba

Wakuta

2008

Psychiatry Clin Neurosci

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“…HVA and MHPG CSF concentrations were inversely correlated with the number of cigarettes smoked/day, while we did not find any significant Association between MAOA, dopamine function and BMI F Ducci et al effect of smoking on 5-HIAA levels (see Table 2). Since the effect of smoking on 5-HIAA has been reported in depressed patients, 43 we examined the effect of smoking versus nonsmoking on 5-HIAA levels. Smokers had lower 5-HIAA (67.1, s.e.…”

Section: Mhpg Csf Mhpg Levels Did Not Differ Between the Two Genotypmentioning

confidence: 99%

A functional polymorphism in the MAOA gene promoter (MAOA-LPR) predicts central dopamine function and body mass index

Ducci¹,

Newman²,

Funt³

et al. 2006

Mol Psychiatry

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Variation in brain monoaminergic activity is heritable and modulates risk of alcoholism and other addictions, as well as food intake and energy expenditure. Monoamine oxidase A deaminates the monoamine neurotransmitters serotonin, dopamine (DA), and noradrenalin. The monoamine oxidase A (MAOA) gene (Xp11.5) contains a length polymorphism in its promoter region (MAOA-LPR) that putatively affects transcriptional efficiency. Our goals were to test (1) whether MAOA-LPR contributes to interindividual variation in monoamine activity, assessed using levels of cerebrospinal fluid (CSF) monoamine metabolites; and (2) whether MAOA-LPR genotype influences alcoholism and/or body mass index (BMI). Male, unrelated criminal alcoholics (N = 278) and controls (N = 227) were collected from a homogeneous Finnish source population. CSF concentration of 5-hydroxyindoleacetic acid (5-HIAA), homovanillic acid (HVA), and 3-methoxy-4-hydroxyphenylglycol (MHPG) were available from 208 participants. Single allele, hemizygous genotypes were grouped according to inferred effect of the MAOA alleles on transcriptional activity. MAOA-LPR genotypes had a significant effect on CSF HVA concentration (P = 0.01) but explained only 3% of the total variance. There was a detectable but nonsignificant genotype effect on 5-HIAA and no effects on MHPG. Specifically, the genotype conferring high MAOA activity was associated with lower HVA levels in both alcoholics and controls, a finding that persisted after accounting for the potential confounds of alcoholism, BMI, height, and smoking. MAOA-LPR genotype predicted BMI (P < 0.005), with the high-activity genotype being associated with lower BMI. MAOA-LPR genotypes were not associated with alcoholism or related psychiatric phenotypes in this data set. Our results suggest that MAOA-LPR allelic variation modulates DA turnover in the CNS, but does so in a manner contrary to our prior expectation that alleles conferring high activity would predict higher HVA levels in CSF. Our results are consistent with an emerging literature that suggests greater complexity in how variation in MAOA expression alters monoaminergic function. Finally, our work suggests that MAOA may be involved in the regulation of BMI. Independent samples are necessary to confirm this preliminary finding.

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“…Prenatal smoking exposure may have a long-term influence on offspring serotonin metabolism. Chronic nicotine exposure reduces serotonin metabolism in animals [16], smokers have reduced serotonin levels in the cerebrospinal fluid [17], and reduced serotonin levels is associated with increased risks of suicidal acts [18]. Using a large population-based data set, we studied the association between maternal smoking during pregnancy and risk of completed suicide and suicidal acts in young offspring after taking family history of psychiatric diseases into account.…”

Section: Introductionmentioning

confidence: 99%

Maternal smoking during pregnancy and risks of suicidal acts in young offspring

et al. 2011

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Word count (excluding title page, abstract, references and tables): 2,976. 2 AbstractObstetric and neonatal complications have been associated with completed and attempted suicide (suicidal acts) in young offspring. Maternal smoking is one of the most important risk factors for obstetric complications, but the association between prenatal smoking exposure and offspring risk of suicidal acts is unknown.We performed a population-based study of 1 449,333 single births born in Sweden between 1983 and 1996, derived from linked registry data. Maternal smoking and risks of suicidal acts in offspring were estimated using hazard ratios, derived from proportional-hazard models, controlling for potential confounding of parental socio-demographic factors and psychiatric care in first degree relatives. To control for unmeasured familial confounding, a matched case-control analysis of suicidal acts was performed within sibling pairs discordant for prenatal smoking exposure.In the cohort analysis, the adjusted hazard ratio for completed suicide among offspring to women smoking 1-9 cigarettes and at least 10 cigarettes per day were 1.67, 95% confidence interval (CI), 1.29-2.16, and 1.54, 95% CI, 1.12-2.10. For suicidal acts, corresponding hazard ratios were 1.28, 95% CI 1.21-1.35 and 1.48, 95% CI 1.39-1.57, respectively. However, in sibling pairs discordant for suicidal acts and prenatal smoking exposure, we found no evidence that prenatal smoking exposure increased the risk of suicidal acts. We conclude that the association between prenatal smoking exposure and offspring risk of suicidal acts is probably confounded by unmeasured familial factors.Word count: 230

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Cigarette Smoking, Suicidal Behavior, and Serotonin Function in Major Psychiatric Disorders

Cited by 245 publications

References 54 publications

Chronic effect of nicotine on serotonin transporter mRNA in the raphe nucleus of rats: Reversal by co‐administration of bupropion

Chronic effect of nicotine on serotonin transporter mRNA in the raphe nucleus of rats: Reversal by co‐administration of bupropion

A functional polymorphism in the MAOA gene promoter (MAOA-LPR) predicts central dopamine function and body mass index

Maternal smoking during pregnancy and risks of suicidal acts in young offspring

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