Biochemical changes, early brain growth suppression and impaired detour learning in nicotine-treated chicks

Pennington, Sam N.; Sandstrom, Lorraine P.; Shibley, Ivan A.; Long, Sheree D.; Beeker, Kelly R.; Smith, Carlton; Lee, Kyung Hwa; Jones, Tabitha; Cummings, Kevin M.; Means, Larry W.

doi:10.1016/0165-3806(94)00135-9

Cited by 23 publications

(15 citation statements)

References 37 publications

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“…Nicotine can readily cross the placental barrier and has been found in the amniotic fluid and umbilical cord of neonates (Luck et al, 1985). Numerous studies have demonstrated that nicotine is the main psychoactive ingredient of tobacco use, as well as a strong growth and neurobehavioral toxicant (Pennington et al, 1994;Ernst et al, 2001;Vaglenova et al, 2004). Our present study showed that nicotine expo-sure during pregnancy resulted in IUGR as shown by a significant reduction in fetal body weight, fetal body and tail lengths that were accompanied by a reduction in maternal body weight.…”

Section: Discussionsupporting

confidence: 59%

Growth retardation of fetal rats exposed to nicotine in utero: Possible involvement of CYP1A1, CYP2E1, and P‐glycoprotein

Wang

Chen

Yan

et al. 2008

Environmental Toxicology

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ABSTRACT:To elucidate the possible metabolic mechanism of intrauterine growth retardation induced by nicotine, this study determines the effects of prenatal nicotine exposure on fetal development and cytochrome P4501A1 (CYP1A1), CYP2E1, and P-glycoprotein (Pgp) expression in maternal liver and placenta. Pregnant rats were given 1.0 mg/kg nicotine subcutaneously twice a day from gestational day (GD) 8 to GD 15, 18, or 21. In nicotine-treated groups, fetal developmental parameters including body weight were significantly lower. The activities of CYP1A1 and CYP2E1 in maternal liver microsomes in nicotine-treated groups increased significantly with progressing gestation when compared with the corresponding control, but returned to the level similar to the control in late pregnancy. Nicotine-treated groups induced pathological changes and increased malondialdehyde (MDA) content in the placenta when compared with the control. The gene expressions of CYP1A1 and CYP2E1 in the placenta increased significantly in nicotine-treated groups on GD 15 and GD 18, but returned to the level similar to the corresponding control on GD 21. In nicotine group, there was a decrease of mdr1a expression on GD 15, GD 18, and GD 21, with the most significant decrease on GD 15. In contrast, no significant difference was found in mdr1b mRNA expression between the nicotine-treated animals and the corresponding control. In comparison with the corresponding control, the placental Pgp protein significantly decreased on GD 15 and GD 18. Our results showed that prenatal nicotine exposure resulted in inhibition of fetal growth significantly. The induction of CYP2E1 and CYP1A1 gene expression by nicotine in the maternal liver and placenta may be involved with the observed increase in oxidative stress and lipid peroxidation. The inhibition of the placental Pgp expression by nicotine may also contribute to an increased susceptibility of the fetus to environmental toxins.

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Section: Discussionsupporting

confidence: 59%

Growth retardation of fetal rats exposed to nicotine in utero: Possible involvement of CYP1A1, CYP2E1, and P‐glycoprotein

Wang

Chen

Yan

et al. 2008

Environmental Toxicology

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“…In humans, maternal smoking has been associated with babies of lower birth weight, increased risk of sudden infant death syndrome, and increased risk of psychiatric disorders in childhood and adolescence (Ernst et al, 2001), including ADHD (Milberger et al, 1996;Milberger et al, 1998). Cognitive impairments and hyperactivity have also been reported in animals exposed to nicotine during development (Genedani et al, 1983;Sorenson et al, 1991;Pennington et al, 1994;Shacka et al, 1997). A blunting of both cholinergic and catecholaminergic function is also seen in rats prenatally exposed to nicotine (Navarro et al, 1988(Navarro et al, , 1989Oliff and Gallardo, 1999).…”

Section: Discussionmentioning

confidence: 99%

Conditional Expression in Corticothalamic Efferents Reveals a Developmental Role for Nicotinic Acetylcholine Receptors in Modulation of Passive Avoidance Behavior

et al. 2003

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Prenatal nicotine exposure has been linked to attention deficit hyperactivity disorder and cognitive impairment, but the sites of action for these effects of nicotine are still under investigation. High-affinity nicotinic acetylcholine receptors (nAChRs) contain the beta2 subunit and modulate passive avoidance (PA) learning in mice. Using an inducible, tetracycline-regulated transgenic system, we generated lines of mice with expression of high-affinity nicotinic receptors restored in specific neuronal populations. One line of mice shows functional beta2 subunit-containing nAChRs localized exclusively in corticothalamic efferents. Functional, presynaptic nAChRs are present in the thalamus of these mice as detected by nicotine-elicited rubidium efflux assays from synaptosomes. Knock-out mice lacking high-affinity nAChRs show elevated baseline PA learning, whereas normal baseline PA behavior is restored in mice with corticothalamic expression of these nAChRs. In contrast, nicotine can enhance PA learning in adult wild-type animals but not in corticothalamic-expressing transgenic mice. When these transgenic mice are treated with doxycycline in adulthood to switch off nAChR expression, baseline PA is maintained even after transgene expression is abolished. These data suggest that high-affinity nAChRs expressed on corticothalamic neurons during development are critical for baseline PA performance and provide a potential neuroanatomical substrate for changes induced by prenatal nicotine exposure leading to long-term behavioral and cognitive deficits.

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“…Perturbations that alter neural proliferation and migration often result in altered differentiation, such as exposure to X-ray irradiation Norton and Donoso, 1985]. Environmental agents that affect differentiation of the nervous system include ethanol [Valles et al, 1996;Laev et al, 1995;Lauder and Schambra, 1999], nicotine [Frischer et al, 1988;Slotkin et al, 1993;Pennington et al, 1994;Cutler et al, 1996;Levitt, 1998;Audesirk and Cabell, 1999], methylmercury [Barone et al, 1998], and lead [Petit and LeBoutillier, 1979;Alfano and Petit, 1982;Petit et al, 1983]. The formation of myelin occurs later in development than proliferation and migration of neuronal populations.…”

Section: How Environmental Factors Influence Central Nervous System Dmentioning

confidence: 97%

Environmental factors associated with a spectrum of neurodevelopmental deficits

Mendola

Selevan

Gutter

et al. 2002

Ment. Retard. Dev. Disabil. Res. Rev.

249

130

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A number of environmental agents have been shown to demonstrate neurotoxic effects either in human or laboratory animal studies. Critical windows of vulnerability to the effects of these agents occur both pre- and postnatally. The nervous system is relatively unique in that different parts are responsible for different functional domains, and these develop at different times (e.g., motor control, sensory, intelligence and attention). In addition, the many cell types in the brain have different windows of vulnerability with varying sensitivities to environmental agents. This review focuses on two environmental agents, lead and methylmercury, to illustrate the neurobehavioral and cognitive effects that can result from early life exposures. Special attention is paid to distinguishing between the effects detected following episodes of poisoning and those detected following lower dose exposures. Perinatal and childhood exposure to high doses of lead results in encephalopathy and convulsions. Lower-dose lead exposures have been associated with impairment in intellectual function and attention. At high levels of prenatal exposure, methylmercury produces mental retardation, cerebral palsy and visual and auditory deficits in children of exposed mothers. At lower levels of methylmercury exposure, the effects in children have been more subtle. Other environmental neurotoxicants that have been shown to produce developmental neurotoxicity include polychlorinated biphenyls (PCBs), dioxins, pesticides, ionizing radiation, environmental tobacco smoke, and maternal use of alcohol, tobacco, marijuana and cocaine. Exposure to environmental agents with neurotoxic effects can result in a spectrum of adverse outcomes from severe mental retardation and disability to more subtle changes in function depending on the timing and dose of the chemical agent.

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Biochemical changes, early brain growth suppression and impaired detour learning in nicotine-treated chicks

Cited by 23 publications

References 37 publications

Growth retardation of fetal rats exposed to nicotine in utero: Possible involvement of CYP1A1, CYP2E1, and P‐glycoprotein

Growth retardation of fetal rats exposed to nicotine in utero: Possible involvement of CYP1A1, CYP2E1, and P‐glycoprotein

Conditional Expression in Corticothalamic Efferents Reveals a Developmental Role for Nicotinic Acetylcholine Receptors in Modulation of Passive Avoidance Behavior

Environmental factors associated with a spectrum of neurodevelopmental deficits

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