Evaluation of emotional behaviors in young offspring of C57BL/6J mice after gestational and/or perinatal exposure to nicotine in six different time-windows

Alkam, Tursun; Kim, Hyoung Chun; Hiramatsu, Masayuki; Mamiya, Takayoshi; Aoyama, Yuki; Nitta, Atsumi; Yamada, Kiyofumi; Nabeshima, Toshitaka

doi:10.1016/j.bbr.2012.10.058

Cited by 53 publications

(53 citation statements)

References 56 publications

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“…This is in contrast to the NIH test, where an aversive environment elicits a passive behavioral response (not approaching and consuming the food), which is indicative of heightened anxiety in the animal. Both ourselves 24, 27, 51 and others 52, 77–79 have utilized these behavioral paradigms to investigate the anxiety-related effects of nicotinic drugs. It is important to note that there may be some developmental effects associated with the polymorphism present in the NRG3 ska mice; however, it is unlikely that these effects account for their anxiolytic phenotype following 24hWD from nicotine.…”

Section: Discussionmentioning

confidence: 99%

Evidence from mouse and man for a role of neuregulin 3 in nicotine dependence

et al. 2013

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Addiction to nicotine and ability to quit smoking are influenced by genetic factors. We used functional genomic approaches (chromatin immunoprecipitation (ChIP) and whole genome sequencing) to identify CREB targets following chronic nicotine administration and withdrawal in rodents. fWe found that chronic nicotine and withdrawal differentially modulate CREB binding to the gene for Neuregulin 3 (NRG3). Quantitative analysis of saline, nicotine, and nicotine withdrawal in two biological replicates corroborate this finding, with NRG3 increases in both mRNA and protein following withdrawal from chronic nicotine treatment. To translate these data for human relevance, single nucleotide polymorphisms (SNPs) across NRG3 were examined for association with prospective smoking cessation among smokers of European ancestry treated with transdermal nicotine in two independent cohorts. Individual SNP and haplotype analysis support association of NRG3 SNPs and smoking cessation success. NRG3 is a neural-enriched member of the EGF family, and a specific ligand for the receptor tyrosine kinase ErbB4, which is also up-regulated following nicotine treatment and withdrawal. Mice with significantly reduced levels of NRG3 or pharmacological inhibition of ErbB4 show similar reductions in anxiety following nicotine withdrawal compared to control animals, suggesting a role for NRG3 in nicotine dependence. While the function of the SNP in NRG3 in humans is not known, these data suggest that Nrg3/ErbB4 signaling may be an important factor in nicotine dependence.

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Section: Discussionmentioning

confidence: 99%

Evidence from mouse and man for a role of neuregulin 3 in nicotine dependence

et al. 2013

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“…Pre‐clinical models, which offer more rigorous control over genetic and environmental variables, consistently show that prenatal nicotine exposure (PNE) produces ADHD‐like phenotypes in rodent models (Schneider et al, 2011; Pauly et al, 2004; Alkam et al, 2013a,b; Zhu et al, 2014, 2012; Hall et al, 2016). Thus, when the human and animal studies are taken together, PNE emerges as a significant environmental risk factor for ADHD even in the absence of genetic predisposition.…”

Section: Introductionmentioning

confidence: 99%

A prenatal nicotine exposure mouse model of methylphenidate responsive ADHD‐associated cognitive phenotypes

Zhu

Fan

McCarthy

et al. 2017

Intl J of Devlp Neuroscience

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Prenatal exposure to nicotine via cigarette smoke or other forms of tobacco use is a significant environmental risk factor for attention deficit hyperactivity disorder (ADHD). The neurobiological mechanisms underlying the link between prenatal nicotine exposure (PNE) and ADHD are not well understood. Animal models, especially rodent models, are beginning to bridge this gap in knowledge. Although ADHD is characterized by hyperactivity, inattention, impulsivity and working memory deficits, the majority of the animal models are based on only one or two ADHD associated phenotypes, in particular, hyperactivity or inattention. We report a PNE mouse model that displays the full range of ADHD associated behavioral phenotypes including working memory deficit, attention deficit and impulsive-like behavior. All of the ADHD-associated phenotypes respond to a single administration of a therapeutic equivalent dose of methylphenidate. In an earlier study, we showed that PNE produces hyperactivity, frontal cortical hypodopaminergic state and thinning of the cingulate cortex. Collectively, these data suggest that the PNE mouse model recapitulates key features of ADHD and may be a suitable preclinical model for ADHD research.

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“…In the present study, we investigated the mechanism by which PNE impairs neurodevelopment, resulting in long-lasting behavioral deficits. We have previously analyzed the plasma cotinine levels, a metabolite of nicotine, in dam and pups on the day of delivery, under the same schedule of PNE employed in the present study (Alkam et al, 2013a). The results suggested that PNE under our experimental condition provided similar levels of plasma nicotine in pregnant dams with those found in typical smokers who absorb systemically about 20 mg nicotine daily on the average United States cigarette consumption of 17 cigarettes per day (Matta et al, 2007).…”

Section: Introductionmentioning

confidence: 52%

“…In rodents, prenatal nicotine exposure (PNE) has been shown to induce abnormal behaviors such as hyperlocomotion (Zhu et al, 2012) and impairment of emotion (Alkam et al, 2013a), cognitive function (Alkam et al, 2013b), and attention (Schneider et al, 2011). Thus, PNE may bring about long-lasting changes in the brain structure and function of the fetus (Dwyer et al, 2009;Pagani, 2014).…”

Section: Introductionmentioning

confidence: 99%

Prenatal Nicotine Exposure Impairs the Proliferation of Neuronal Progenitors, Leading to Fewer Glutamatergic Neurons in the Medial Prefrontal Cortex

Aoyama

Toriumi

Mouri

et al. 2015

Neuropsychopharmacol

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Cigarette smoking during pregnancy is associated with various disabilities in the offspring such as attention deficit/hyperactivity disorder, learning disabilities, and persistent anxiety. We have reported that nicotine exposure in female mice during pregnancy, in particular from embryonic day 14 (E14) to postnatal day 0 (P0), induces long-lasting behavioral deficits in offspring. However, the mechanism by which prenatal nicotine exposure (PNE) affects neurodevelopment, resulting in behavioral deficits, has remained unclear. Here, we report that PNE disrupted the proliferation of neuronal progenitors, leading to a decrease in the progenitor pool in the ventricular and subventricular zones. In addition, using a cumulative 5-bromo-2 0 -deoxyuridine labeling assay, we evaluated the rate of cell cycle progression causing the impairment of neuronal progenitor proliferation, and uncovered anomalous cell cycle kinetics in mice with PNE. Accordingly, the density of glutamatergic neurons in the medial prefrontal cortex (medial PFC) was reduced, implying glutamatergic dysregulation. Mice with PNE exhibited behavioral impairments in attentional function and behavioral flexibility in adulthood, and the deficits were ameliorated by microinjection of D-cycloserine into the PFC. Collectively, our findings suggest that PNE affects the proliferation and maturation of progenitor cells to glutamatergic neuron during neurodevelopment in the medial PFC, which may be associated with cognitive deficits in the offspring.

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Evaluation of emotional behaviors in young offspring of C57BL/6J mice after gestational and/or perinatal exposure to nicotine in six different time-windows

Cited by 53 publications

References 56 publications

Evidence from mouse and man for a role of neuregulin 3 in nicotine dependence

Evidence from mouse and man for a role of neuregulin 3 in nicotine dependence

A prenatal nicotine exposure mouse model of methylphenidate responsive ADHD‐associated cognitive phenotypes

Prenatal Nicotine Exposure Impairs the Proliferation of Neuronal Progenitors, Leading to Fewer Glutamatergic Neurons in the Medial Prefrontal Cortex

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