Exposure to threshold doses of nicotine : I. Neuroendocrine response to restraint stress in adult male offspring

Poland, Russell E.; Lutchmansingh, Preetam; Au, Denise; Edelstein, M.; Lydecker, Susan; Hsieh, Chrissy; McCracken, James T.

doi:10.1016/0024-3205(94)00318-1

Cited by 15 publications

(8 citation statements)

References 27 publications

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“…Future studies are needed to replicate patterns of associations between MSDP, NR3C1 , and newborn neurobehavior. Associations between NR3C1 methylation and both MSDP and infant neurobehavioral development complement preclinical studies showing effects of prenatal nicotine on maternal glucocorticoids and offspring HPA stress response (Chen et al., ; Poland et al., ), and human studies showing effects of MSDP on maternal and fetal (cord blood) glucocorticoids and offspring HPA stress response, including effects on offspring cortisol in the current subsample (Schuetze et al., ; Stroud, Papandonatos, Rodriguez, et al., ; Stroud, Papandonatos, Shenassa, et al., ; Varvarigou et al., ). Results extend prior research through investigating placental glucocorticoid pathways linking MSDP and infant neurobehavior (vs. cortisol response).…”

Section: Discussionsupporting

confidence: 57%

“…We propose that MSDP acts as an intrauterine stressor that alters the maternal–placental–fetal neuroendocrine milieu and “programs” alterations in offspring neurobehavior via glucocorticoid pathways. Supporting this proposal, preclinical models have revealed associations between prenatal nicotine exposure and alterations in maternal glucocorticoids and offspring hypothalamic–pituitary–adrenal (HPA) stress response (Chen et al., ; Poland et al., ). Human studies have confirmed increased cortisol in the cord blood of MSDP‐exposed offspring (McDonald et al., ; Varvarigou, Petsali, Vassilakos, & Beratis, ), associations between MSDP and infant cortisol stress response (Schuetze, Lopez, Granger, & Eiden, ; Stroud, Papandonatos, Rodriguez, et al., ), and perinatal glucocorticoid programming of nicotine dependence in adult offspring (Stroud, Papandonatos, Shenassa, et al., ).…”

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confidence: 99%

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Epigenetic Regulation of Placental NR3C1: Mechanism Underlying Prenatal Programming of Infant Neurobehavior by Maternal Smoking?

et al. 2016

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Epigenetic regulation of the placental glucocorticoid receptor gene (NR3C1) was investigated as a mechanism underlying links between maternal smoking during pregnancy (MSDP) and infant neurobehavior in 45 mother-infant pairs (49% MSDP-exposed; 52% minorities; ages 18-35). The NICU Network Neurobehavioral Scale was administered 7 times over the first postnatal month; methylation of placental NR3C1 was assessed via bisulfite pyrosequencing. Increased placental NR3C1 methylation was associated with increased infant attention and self-regulation, and decreased lethargy and need for examiner soothing over the first postnatal month. A causal steps approach revealed that NR3C1 methylation and MSDP were independently associated with lethargic behavior. Although preliminary, results highlight the importance of epigenetic mechanisms in elucidating pathways to neurobehavioral alterations from MSDP.

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Section: Discussionsupporting

confidence: 57%

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confidence: 99%

Epigenetic Regulation of Placental NR3C1: Mechanism Underlying Prenatal Programming of Infant Neurobehavior by Maternal Smoking?

et al. 2016

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“…In the present study, we test the hypothesis that exposure to MSDP will be associated with persistent dysregulation, or programming, of the offspring HPA axis over the neonatal period. The plausibility of our hypothesis is supported by preclinical studies showing increased HPA stress response in prenatal nicotine-exposed offspring, and human studies demonstrating increased cord blood cortisol in MSDP-exposed offspring (Poland et al, 1994a; Poland et al, 1994b; Poland et al, 1996; McDonald et al, 2006; Varvarigou et al, 2006; Varvarigou et al, 2009). Further and most relevant, Ramsay et al (1996) found increased baseline and attenuated response to inoculation at two months in MSDP and low-level alcohol-exposed infants, while Schuetze et al (2008) showed increased peak cortisol response to stressful behavioral tasks in MSDP-exposed infants at seven months.…”

Section: Introductionsupporting

confidence: 54%

Maternal smoking during pregnancy and infant stress response: Test of a prenatal programming hypothesis

Stroud

Papandonatos

Rodriguez

et al. 2014

Psychoneuroendocrinology

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Background Maternal smoking during pregnancy (MSDP) is associated with early and long-term neurobehavioral deficits; however mechanisms remain unknown. We tested the hypothesis that MSDP programs the hypothalamic pituitary adrenocortical (HPA) axis of the offspring leading to adverse outcomes. In an intensive, prospective study, we investigated associations between MSDP and infant cortisol stress response and explored whether alterations in cortisol response were mediated by epigenetic modulation of the placental glucocorticoid receptor gene (NR3C1). Methods Participants were 100 healthy mother-infant pairs (53% MSDP-exposed; 42% female) from a low income, racially/ethnically diverse sample (55% minorities). MSDP was assessed by timeline followback interview verified by saliva and meconium cotinine. Infant cortisol responses to a neurobehavioral exam were assessed 7 times over the first postnatal month. Methylation of placental NR3C1 promoter exon 1F was assessed using bisulfite pyrosequencing in a subsample (n=45). Results MSDP-exposed infants showed significantly and persistently attenuated basal and reactive cortisol levels over the first postnatal month vs. unexposed infants. Exploratory analyses revealed that MSDP was associated with altered methylation of the placental NR3C1 promoter; degree of methylation of the placental NR3C1 was associated with infant basal and reactive cortisol over the first postnatal month and mediated effects of MSDP on infant basal cortisol. Conclusions Results provide initial support for our hypothesis that MSDP programs offspring HPA (dys) regulation. Epigenetic regulation of placental GR may serve as a novel underlying mechanism. Results may have implications for delineating pathways to adverse outcomes from MSDP.

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“…Serum corticosterone was analyzed by radioimmunoassay, as previously described (Poland et al, 1994). Briefly, corticosterone was measured using anticorticosterone antisera and I-125 corticosterone obtained form ICN Biomedicals.…”

Section: Corticosterone Assaymentioning

confidence: 99%

Total Sleep Deprivation Decreases Immobility In The Forced-Swim Test

Rodríguez

Kim

Poland

2004

Neuropsychopharmacol

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Sleep deprivation can exert antidepressant effects in humans in less than 24 h, making it the fastest acting antidepressant treatment. However, it is rarely used clinically because the effect disappears once the subject goes back to sleep. An understanding of the neurobiological mechanisms underlying the antidepressant effect of sleep deprivation should help to develop new rapidly acting antidepressant strategies. In the present report, an animal model of depression (the forced-swim test) was used to determine whether the effects of total sleep deprivation parallel those obtained with antidepressant drugs. Using the disk-over-water method, rats deprived of sleep for 24 h exhibited increased swimming behavior when compared to cage control rats, mimicking the effects of serotonergic antidepressants. After 48 h, sleep-deprived rats exhibited increased swimming when compared to both cage control and stimulus control rats, demonstrating that the effect is due to sleep deprivation per se, and not to extraneous factors inherent in the sleep deprivation protocol (such as stress and movement). We believe that this paradigm can be used to study the neurobiological mechanisms of rapid antidepressant effects induced by sleep deprivation.

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Exposure to threshold doses of nicotine : I. Neuroendocrine response to restraint stress in adult male offspring

Cited by 15 publications

References 27 publications

Epigenetic Regulation of Placental NR3C1: Mechanism Underlying Prenatal Programming of Infant Neurobehavior by Maternal Smoking?

Epigenetic Regulation of Placental NR3C1: Mechanism Underlying Prenatal Programming of Infant Neurobehavior by Maternal Smoking?

Maternal smoking during pregnancy and infant stress response: Test of a prenatal programming hypothesis

Total Sleep Deprivation Decreases Immobility In The Forced-Swim Test

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