Higher Rates of Cigarette Smoking in Male Adolescents Before the Onset of Schizophrenia: A Historical-Prospective Cohort Study

Weiser, Mark; Reichenberg, Abraham; Grotto, Itamar; Yasvitzky, R.; Rabinowitz, Jonathan; Lubin, Gad; Nahon, Daniella; Knobler, Haim Y.; Davidson, Michael

doi:10.1176/appi.ajp.161.7.1219

Cited by 151 publications

(112 citation statements)

References 51 publications

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“…Smoking and neuropsychiatric disease often co-occur, with the onset of both disorders emerging during adolescence (Covey et al, 2008;Gehricke et al, 2007;Weiser et al, 2004). The adolescent brain undergoes dynamic maturation of limbic circuitry and of efferent dopamine (DA) and serotonin (5-HT) neurotransmitter systems, which are common components that underlie the rewarding aspects of smoking, as well as neuropsychiatric pathologies.…”

Section: Introductionmentioning

confidence: 99%

Nicotine Alters Limbic Function in Adolescent Rat by a 5-HT1A Receptor Mechanism

Dao

McQuown

Loughlin

et al. 2011

Neuropsychopharmacol

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Epidemiological studies have shown that adolescent smoking is associated with health risk behaviors, including high-risk sexual activity and illicit drug use. Using rat as an animal model, we evaluated the behavioral and biochemical effects of a 4-day, low-dose nicotine pretreatment (60 mg/kg; intravenous) during adolescence and adulthood. Nicotine pretreatment significantly increased initial acquisition of cocaine self-administration, quinpirole-induced locomotor activity, and penile erection in adolescent rats, aged postnatal day (P)32. These effects were long lasting, remaining evident 10 days after the last nicotine treatment, and were observed when nicotine pretreatment was administered during early adolescence (P28-31), but not late adolescence (P38-41) or adulthood (P86-89). Neurochemical analyses of c-fos mRNA expression, and of monoamine transmitter and transporter levels, showed that forebrain limbic systems are continuing to develop during early adolescence, and that this maturation is critically altered by brief nicotine exposure. Nicotine selectively increased c-fos mRNA expression in the nucleus accumbens shell and basolateral amygdala in adolescent, but not adult animals, and altered serotonin markers in these regions as well as the prefrontal cortex. Nicotine enhancement of cocaine self-administration and quinpirole-induced locomotor activity was blocked by co-administration of WAY 100 635 (N-{2-[4-(2-methoxyphenyl)-1-piperazinyl] ethyl}-N-(2-pyridinyl)cyclohexanecarboxamide), a selective serotonin 1A (5-HT1A) receptor antagonist. Early adolescent pretreatment with the mixed autoreceptor/heteroceptor 5-HT1A receptor agonist, 8-OH-DPAT, but not the autoreceptor-selective agonist, S-15535, also enhanced quinpirole-induced locomotor activation. Nicotine enhancement of quinpirole-induced penile erection was not blocked by WAY 100 635 nor mimicked by 8-OH-DPAT. These findings indicate that early adolescent nicotine exposure uniquely alters limbic function by both 5-HT1A and non-5-HT1A receptor mechanisms.

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Section: Introductionmentioning

confidence: 99%

Nicotine Alters Limbic Function in Adolescent Rat by a 5-HT1A Receptor Mechanism

Dao

McQuown

Loughlin

et al. 2011

Neuropsychopharmacol

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“…These risk factors could act as a second "hit" that contributes to the emergence of the illness in a genetically vulnerable individual. Obstetrical complications have long been associated with schizophrenia and likely represent a risk factor for the illness that is relevant in combination with other factors [18]. In a sample of 55 subjects at-risk for psychosis, we (unpublished data) found that 21 (41%) reported a history of definite obstetrical complications as per the Lewis Obstetric Complications Scale compared with six (14%) of 41 normal comparison subjects.…”

Section: Environmental Risk Factorsmentioning

confidence: 79%

“…Aside from the clinical and genetic risk factors, there are several known environmental risk factors for schizophrenia that have been further elucidated in recent reviews [16][17][18]. These risk factors could act as a second "hit" that contributes to the emergence of the illness in a genetically vulnerable individual.…”

Section: Environmental Risk Factorsmentioning

confidence: 99%

“…Other factors, including urban dwelling and immigration, have been found to increase risk for schizophrenia approximately 1.5 to almost three-fold, with speculation that poverty and poor nutrition and health may account for these effects [20]. Substance abuse, especially cannabis abuse in early adolescence, in addition to nicotine use, is associated with a twofold increase in risk [18,21]. Recently, we [3] have reported that at-risk subjects who later converted to psychosis at 1-year follow-up were more likely to have abused substances before the onset of psychosis.…”

Section: Environmental Risk Factorsmentioning

confidence: 99%

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Progress in the prospective study of the schizophrenia prodrome

Fu¹,

Cadenhead

2005

Current Psychosis & Therapeutics Reports

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Further understanding of the schizophrenia spectrum has helped to define the prodrome of the illness, leading to hopes of earlier identification and intervention in susceptible, at-risk individuals. Given the heterogeneity and comorbidity observed in the clinically and demographically identified prodromal sample, it is essential that neurobiological markers that are more closely linked to brain function, and perhaps the ability to predict evolution of psychosis, be identified. Ultimately, it may be possible to identify an algorithm of risk factors that will combine clinical and demographic risk factors with vulnerability markers associated with later development of schizophrenia to better target at-risk individuals or preventative treatment.

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“…have a similar effect in improving attentional performance in people with schizophrenia who were taking antipsychotic drugs [22][23][24]. Interestingly, higher smoking rates appear to precede the onset of schizophrenia [25]. This may be also related to self-medication for cognitive deficits, which are present before the first break into schizophrenia.…”

Section: Nicotinic Systems and The Cognitive Impairment Of Schizophreniamentioning

confidence: 94%

Nicotinic interactions with antipsychotic drugs, models of schizophrenia and impacts on cognitive function

Levin

Rezvani

2007

Biochemical Pharmacology

109

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People with schizophrenia often have substantial cognitive impairments, which may be related to nicotinic receptor deficits, (α7 and α4β2), documented in the brains of people with schizophrenia. The large majority of people with schizophrenia smoke cigarettes. Thus, nicotinic interactions with antipsychotic drugs are widespread. Complementary co-therapies of novel nicotinic ligands are being developed to add to antipsychotic therapy to treat the cognitive impairment of schizophrenia. Thus, it is critical to understand the interaction between nicotinic treatments and antipsychotic drugs. Nicotinic interactions with antipsychotic drugs, are complex since both nicotine and antipsychotics have complex actions. Nicotine stimulates and desensitizes nicotinic receptors of various subtypes and potentiates the release of different neurotransmitters. Antipsychotics also act on a verity of receptor systems. For example, clozapine acts as an antagonist at a variety of neurotransmitter receptors such as those for dopamine, serotonin, norepinepherine and histamine. In a series of studies, we have found that in normally functioning rats, moderate doses of clozapine impair working memory and that clozapine blocks nicotine-induced memory and attentional improvement. Clozapine and nicotine can attenuate each other's beneficial effects in reversing the memory impairment caused by the psychototmimetic drug dizocilpine. A key to the clozapine-induced attenuation of nicotineinduced cognitive improvement appears to be its 5HT 2 antagonist properties. The selective 5HT 2 antagonist ketanserin has a similar action of blocking nicotine-induced memory and attentional improvements. It is important to consider the interactions between nicotinic and antipsychotic drugs to develop the most efficacious treatment for cognitive improvement in people with schizophrenia.

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Higher Rates of Cigarette Smoking in Male Adolescents Before the Onset of Schizophrenia: A Historical-Prospective Cohort Study

Cited by 151 publications

References 51 publications

Nicotine Alters Limbic Function in Adolescent Rat by a 5-HT1A Receptor Mechanism

Nicotine Alters Limbic Function in Adolescent Rat by a 5-HT1A Receptor Mechanism

Progress in the prospective study of the schizophrenia prodrome

Nicotinic interactions with antipsychotic drugs, models of schizophrenia and impacts on cognitive function

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