Nicotine exposure throughout early development promotes nicotine self-administration in adolescent mice and induces long-lasting behavioural changes

Chistyakov, Vladimir; Patkina, N.A.; Tammimäki, Anne; Talka, Reeta; Salminen, Outi; Belozertseva, Irina; Galankin, T.; Tuominen, Raimo K.; Zvartau, Edwin

doi:10.1016/j.ejphar.2010.04.044

Cited by 28 publications

(33 citation statements)

References 37 publications

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“…In fact, evidence exists that prenatal nicotine increases anxiety in rodents (Huang et al, 2007;Santiago and Huffman, 2013;Vaglenova et al, 2008), although also see Amos-Kroohs et al (2013). Exposed animals are more likely to self-administer nicotine later in life (Chistyakov et al, 2010;Levin et al, 2006). Others have shown that exposed rodents are more sensitive to the rewarding (Harrod et al, 2012) and locomotor-stimulating (Amos-Kroohs et al, 2013) properties of METH.…”

Section: Tobacco/nicotinementioning

confidence: 99%

Developmental Consequences of Fetal Exposure to Drugs: What We Know and What We Still Must Learn

Ross

Graham

Money

et al. 2014

Neuropsychopharmacol

331

241

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Most drugs of abuse easily cross the placenta and can affect fetal brain development. In utero exposures to drugs thus can have long-lasting implications for brain structure and function. These effects on the developing nervous system, before homeostatic regulatory mechanisms are properly calibrated, often differ from their effects on mature systems. In this review, we describe current knowledge on how alcohol, nicotine, cocaine, amphetamine, Ecstasy, and opiates (among other drugs) produce alterations in neurodevelopmental trajectory. We focus both on animal models and available clinical and imaging data from cross-sectional and longitudinal human studies. Early studies of fetal exposures focused on classic teratological methods that are insufficient for revealing more subtle effects that are nevertheless very behaviorally relevant. Modern mechanistic approaches have informed us greatly as to how to potentially ameliorate the induced deficits in brain formation and function, but conclude that better delineation of sensitive periods, dose-response relationships, and long-term longitudinal studies assessing future risk of offspring to exhibit learning disabilities, mental health disorders, and limited neural adaptations are crucial to limit the societal impact of these exposures.

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Section: Tobacco/nicotinementioning

confidence: 99%

Developmental Consequences of Fetal Exposure to Drugs: What We Know and What We Still Must Learn

Ross

Graham

Money

et al. 2014

Neuropsychopharmacol

331

241

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“…(B2) Ankarberg et al 2001Ankarberg et al , 2004Eriksson et al 2000;Fredriksson et al 2000;Frischer et al 1988;Gilbertson and Barron 2005;King and Strand 1988. (B3) Chistyakov et al 2010;Gaworski et al 2004;Martin and Martin 1981;Newman et al 1999;Romero and Chen 2004;Tizabi et al 1997. (C1) King and Strand 1988;LeSage et al 2006;Pauly et al 2004;Peters and Tang 1982;Schlumpf et al 1988;Vaglenova et al 2004.…”

Section: Exposure Period (Species Combined) (A) Increased (B) Not Affmentioning

confidence: 98%

“…(B1) Frischer et al 1988;Gaworski et al 2004;King and Strand 1988;Newman et al 1999;Paulson et al 1993;Schlumpf et al 1988;Shacka et al 1997. (B2) Ankarberg et al 2001Ankarberg et al , 2004Chistyakov et al 2010;Eriksson et al 2000;Franke et al 2007;Fredriksson et al 2000;Paulson et al 1993;Pauly et al 2004;Romero and Chen 2004. (B3) Ankarberg et al 2001Ankarberg et al , 2004Eriksson et al 2000;Fredriksson et al 2000;Martin and Martin 1981;Sobrian et al 2003Sobrian et al , 2008 (C1) Gilbertson and Barron 2005;King and Strand 1988;LeSage et al 2006;Schlumpf et al 1988.…”

Section: Age At Testing (A) Increased (B) Not Affected (C) Decreasedmentioning

confidence: 98%

“…Thirteen studies assessed the effects of drug challenges (predominantly nicotine) on rats (7 studies) or mice (6) exposed to nicotine early in development (Abreu-Villaça et al 2004a;Ankarberg et al 2001Ankarberg et al , 2004Chistyakov et al 2010;Eriksson et al 2000;Fredriksson et al 2000;Pauly et al 2004;Seidler et al 1992;Shacka et al 1997;Slotkin et al 2006;Sobrian et al 2003Sobrian et al , 2008Zbuzek and Chin 1994). Six studies used only male offspring, another six used both sexes, and one did not specify the sex of animals.…”

Section: Response To Drug Challengementioning

confidence: 98%

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Effects of Pre- and Neonatal Nicotine Exposure in Rodents: Inconsistent Evidence

Sobrian¹,

Holson²

2011

ILAR Journal

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This review presents an analysis of the literature on behavioral effects of developmental exposure to nicotine, as assessed in rodent models that mimic the consequences for human offspring of maternal cigarette smoking. Despite the frequency of reports of low birth weight, hyperactivity, cognitive deficits, and psychiatric problems, inconsistencies exist in both the clinical and experimental literature. Confounding socioeconomic and other demographic variables may account for discrepancies in clinical reports, and the choice of developmental exposure period and the method of nicotine administration may explain differences in experimental outcomes. Analysis of a number of variables (e.g., physical, behavioral, and cognitive) shows that fetal exposure to nicotine does not consistently cause growth retardation or decreased birth weight, nor reliably affect motor activity. But combined pre- and neonatal exposure is likely to result in delayed reflex development, global impairments in learning and memory, and an increased incidence of symptoms that model psychiatric illness. There is also support for increased self-administration of nicotine and other drugs of abuse in animals exposed developmentally to nicotine, as well as potent effects on offspring responses to drug challenges. Unlike reports in the clinical literature, sexually dimorphic effects were not evident in most animal models. Possible neuroanatomical and cholinergic mechanisms responsible for behavioral changes are briefly discussed. Statistical and design considerations are provided to increase the translational value of this research and, most importantly, enhance the replicability of reported findings.

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“…Here, we used a mouse model of intracranial nicotine self-administration (ICSA) based on spatial discrimination and voluntary drug intake in naive subjects, which has been proven to be very effective to detect pharmacologically or genetically induced changes in nicotine reward , Maskos et al 2005). Studies using intravenous nicotine self-administration in mice commonly report one single self-administration session (Pons et al 2008;Chistyakov et al 2010) or operate a chronic self-administration procedure by applying priming injections of nicotine to facilitate the acquisition (Metaxas et al 2010;Plaza-Zabala et al 2010). In other studies, mice are first trained to self-administer food (Bilkei-Gorzo et al 2008) or cocaine (Picciotto et al 1998) before switching to nicotine.…”

Section: Involvement Of α7*nachrs In Nicotine Rewardmentioning

confidence: 98%

Alpha7-nicotinic receptors modulate nicotine-induced reinforcement and extracellular dopamine outflow in the mesolimbic system in mice

et al. 2011

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Nicotine exposure throughout early development promotes nicotine self-administration in adolescent mice and induces long-lasting behavioural changes

Cited by 28 publications

References 37 publications

Developmental Consequences of Fetal Exposure to Drugs: What We Know and What We Still Must Learn

Developmental Consequences of Fetal Exposure to Drugs: What We Know and What We Still Must Learn

Effects of Pre- and Neonatal Nicotine Exposure in Rodents: Inconsistent Evidence

Alpha7-nicotinic receptors modulate nicotine-induced reinforcement and extracellular dopamine outflow in the mesolimbic system in mice

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