Smoking during early pregnancy affects the expression pattern of both nicotinic and muscarinic acetylcholine receptors in human first trimester brainstem and cerebellum

Falk, Lena; Nordberg, Agneta; Seiger, Åke; Kjældgaard, A.; Hellström‐Lindahl, Ewa

doi:10.1016/j.neuroscience.2004.12.049

Cited by 67 publications

(54 citation statements)

References 175 publications

(230 reference statements)

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“…Although a previous study has shown that fetal exposure to nicotine increases nAChRs binding sites (Falk et al, 2005), to our knowledge, the present study was the first to demonstrate that chronic exposure to nicotine for different gestational periods differentially regulated nAChR subunits expression pattern in fetal forebrain and hindbrain. Heteromeric and homomeric nAChRs are widely distributed in the embryonic brain, and play a role in the maturation of brain structures during development.…”

Section: Discussioncontrasting

confidence: 53%

The effect of prenatal nicotine on expression of nicotine receptor subunits in the fetal brain

Mao

Zhu

et al. 2008

NeuroToxicology

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Previous studies have suggested that prenatal exposure to nicotine is associated with abnormal development in fetuses, including fetal brain damage. The present study determined the effect of maternal administration of nicotine during different gestational periods on brain nicotine receptor subunits in fetal rats. Subcutaneous injections of nicotine in maternal rats from the early and middle gestation decreased fetal blood PO 2 , increased fetal blood PCO 2 and hemoglobin, and decreased fetal brain weight. The nicotinic acetylcholine receptor (nAChRs) mRNA abundance in the fetal brain was significantly changed by prenatal treatment with nicotine during pregnancy. Fetal α2, α4, α7, and β2 units were significantly increased in the brain by prenatal exposure to nicotine in rat fetuses. However, the expression of mRNA of fetal brain α3, α5, β3, and β4 units were not changed. The results showed that prenatal nicotine can change the development of both α and β subunits of nAChRs in the fetal brain at gene level in association with restriction of fetal brain growth and in utero hypoxia.

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Section: Discussioncontrasting

confidence: 53%

The effect of prenatal nicotine on expression of nicotine receptor subunits in the fetal brain

Mao

Zhu

et al. 2008

NeuroToxicology

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“…74,75 In first-trimester human fetuses, abnormal nicotinic receptor subunit levels have also been detected in the brainstem regions associated with sudden infant death syndrome. 76 Dysfunction of these brainstem regions, which can be associated with sudden infant death syndrome, is strongly associated with maternal cigarette use during pregnancy, and the alterations that are seen with gene expression in these cholinergic receptor subunits may be a contributing factor to the brainstem abnormalities seen in these infants. 77 These molecular alterations in gene expression as a result of prenatal nicotine exposure may be explained by epigenetic mechanisms, which is currently an area of active research.…”

Section: Health Consequences Of Exposure To Nicotinementioning

confidence: 99%

Nicotine and Tobacco as Substances of Abuse in Children and Adolescents

Siqueira¹,

Ryan²,

Gonzalez³

et al. 2017

Pediatrics

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Nicotine is the primary pharmacologic component of tobacco, and users of tobacco products seek out its effects. The highly addictive nature of nicotine is responsible for its widespread use and difficulty with quitting. This technical report focuses on nicotine and discusses the stages of use in progression to dependence on nicotine-containing products; the physiologic characteristics, neurobiology, metabolism, pharmacogenetics, and health effects of nicotine; and acute nicotine toxicity. Finally, some newer approaches to cessation are noted.

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“…Yet in the developing nervous system, very early in gestation, nAChRs are expressed prior to the formation of the neurons, which later establish synaptic contact with the nAChRs. By modifying the function of these receptors, nicotine can interfere with the normal developmental role of ACh (Falk, Nordberg, Seiger, Kjaeldgaard, & Hellstrom-Lindahl, 2005). These effects occur in the range of amounts of nicotine derived from smoking or equivalent sources.…”

Section: A Brief Synopsis Of Nicotine Actionmentioning

confidence: 99%

Critical Review

Ginzel¹,

Maritz

Marks

et al. 2007

J Health Psychol

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The recent expansion of Nicotine Replacement Therapy to pregnant women and children ignores the fact that nicotine impairs, disrupts, duplicates and/or interacts with essential physiological functions and is involved in tobacco-related carcinogenesis. The main concerns in the present context are its fetotoxicity and neuroteratogenicity that can cause cognitive, affective and behavioral disorders in children born to mothers exposed to nicotine during pregnancy, and the detrimental effects of nicotine on the growing organism. Hence, the use of nicotine, whose efficacy in treating nicotine addiction is controversial even in adults, must be strictly avoided in pregnancy, breastfeeding, childhood and adolescence.

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Smoking during early pregnancy affects the expression pattern of both nicotinic and muscarinic acetylcholine receptors in human first trimester brainstem and cerebellum

Cited by 67 publications

References 175 publications

The effect of prenatal nicotine on expression of nicotine receptor subunits in the fetal brain

The effect of prenatal nicotine on expression of nicotine receptor subunits in the fetal brain

Nicotine and Tobacco as Substances of Abuse in Children and Adolescents

Critical Review

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