An animal model of adolescent nicotine exposure: effects on gene expression and macromolecular constituents in rat brain regions

Trauth, Jennifer A; Seidler, Frederic J.; Slotkin, Theodore A.

doi:10.1016/s0006-8993(00)02208-3

Cited by 182 publications

(154 citation statements)

References 58 publications

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“…The nicotine exposure period thus spans the recognized boundaries of adolescence in the rat, as typified by endocrine, pubertal, and behavioral parameters (Spear, 2000). In the adolescent rat this paradigm produces plasma nicotine levels of 25 ng/ ml, similar to that in typical smokers (Lichtensteiger et al, 1988;Trauth et al, 2000b); it produces a transient (10%) reduction in body weight during treatment, an effect that disappears after termination of the infusion (Abreu-Villaça et al, 2003a;Trauth et al, 1999). Studies were conducted at four time points, one during adolescent nicotine administration (PN45) and three during the withdrawal period (PN50, PN60, and PN75).…”

Section: Animals and Nicotine Infusionsmentioning

confidence: 98%

“…On PN30, each animal was implanted with a minipump (Alzet type 1002) as already described, again set to deliver either vehicle or nicotine at an initial dose rate of 6 mg/kg per day, with the infusion terminating during PN47 (Slotkin, 1998;Trauth et al, 1999Trauth et al, , 2000b. The nicotine exposure period thus spans the recognized boundaries of adolescence in the rat, as typified by endocrine, pubertal, and behavioral parameters (Spear, 2000).…”

Section: Animals and Nicotine Infusionsmentioning

confidence: 99%

“…Studies were conducted at four time points, one during adolescent nicotine administration (PN45) and three during the withdrawal period (PN50, PN60, and PN75). Animals were decapitated and the cerebral cortex, midbrain, and hippocampus were dissected (Trauth et al, 2000b), frozen in liquid nitrogen, and stored at À451C until assayed. For each treatment group, 12 animals were examined at each age point, equally divided into males and females.…”

Section: Animals and Nicotine Infusionsmentioning

confidence: 99%

“…The assay for DNA has been described in detail in a previous publication (Trauth et al, 2000b). Briefly, DNA was determined in aliquots of the original tissue homogenate using a modified (Trauth et al, 2000b) fluorescent dyebinding method (Labarca and Piagen, 1980).…”

Section: Tissue Preparation and Assaysmentioning

confidence: 99%

“…Briefly, DNA was determined in aliquots of the original tissue homogenate using a modified (Trauth et al, 2000b) fluorescent dyebinding method (Labarca and Piagen, 1980). Tissues were diluted in 100 mM NaCl, 1 mM EDTA, and 10 mM Tris HCl (pH 7.4) and sonicated for 30 s (Virsonic Cell Disrupter, Virtis, Gardiner, NY).…”

Section: Tissue Preparation and Assaysmentioning

confidence: 99%

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Does Prenatal Nicotine Exposure Sensitize the Brain to Nicotine-Induced Neurotoxicity in Adolescence?

Abreu‐Villaça

Seidler

Slotkin

2004

Neuropsychopharmacol

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Offspring of women who smoke during pregnancy are themselves more likely to take up smoking in adolescence. We evaluated neurotoxicant effects of prenatal and adolescent nicotine exposure in developing rats to evaluate whether these contribute to a biological basis for this relationship. Rats were given nicotine or vehicle throughout pregnancy and the offspring then again received nicotine or vehicle during adolescence (postnatal days PN30-47.5); this regimen reproduces the plasma nicotine levels found in smokers. Indices of neural cell number (DNA concentration and content), cell size (protein/DNA ratio), and cell membrane surface area (membrane/total protein) were then evaluated in brain regions during adolescent nicotine administration (PN45) and up to 1 month post-treatment. By itself, prenatal nicotine administration produced cellular alterations that persisted into adolescence, characterized by net cell losses in the midbrain and to a lesser extent, in the cerebral cortex, with corresponding elevations in the membrane/total protein ratio. The hippocampus showed a unique response, with increased DNA content and regional enlargement. Adolescent nicotine treatment alone had similar, albeit smaller effects, but also showed sex-dependence, with effects on protein biomarkers preferential to females. When animals exposed to nicotine prenatally were then given nicotine in adolescence, the net outcome was worsened, largely representing summation of the two individual effects. Our results indicate that prenatal nicotine exposure alters parameters of cell development lasting into adolescence, where the effects add to those elicited directly by adolescent nicotine; neurotoxicant actions may thus contribute to the association between maternal smoking and subsequent smoking in the offspring.

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Section: Animals and Nicotine Infusionsmentioning

confidence: 98%

Section: Animals and Nicotine Infusionsmentioning

confidence: 99%

Section: Animals and Nicotine Infusionsmentioning

confidence: 99%

Section: Tissue Preparation and Assaysmentioning

confidence: 99%

Section: Tissue Preparation and Assaysmentioning

confidence: 99%

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Does Prenatal Nicotine Exposure Sensitize the Brain to Nicotine-Induced Neurotoxicity in Adolescence?

Abreu‐Villaça

Seidler

Slotkin

2004

Neuropsychopharmacol

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Gestational exposure to nicotine and/or benzo[a]pyrene causes long‐lasting neurobehavioral consequences

Hawkey

Junaid

Yao

et al. 2019

Birth Defects Research

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Tobacco smoke is a complex mixture that includes thousands of compounds. Previously, we have found that gestational exposure to the complex mixture of tobacco smoke extract caused long‐term neurobehavioral impairments. In this study, we examined the interaction of two of the most biologically active, nicotine and benzo[a]pyrene (BaP). Developmental effects were determined in Sprague–Dawley rats prenatally exposed to low doses of BaP and nicotine (0.03 mg/kg/day of BaP and 2 mg/kg/day of nicotine) via maternal osmotic minipumps throughout gestation. Behavioral function was assessed in the offspring via a battery of tests through adolescence into adulthood. There were sex‐selective effects in four of the behavioral tests. In the elevated plus maze, there was a significant interaction of BaP and sex, where BaP‐treated males showed a trend for increased activity. In the novelty suppressed feeding test, there were significant sex selective effects in males such that the normal sex difference in the behavior in this test was eliminated. Male offspring with prenatal exposure to either nicotine or BaP showed significant reductions in fear response. In the Figure‐8 locomotor activity test, BAP‐exposed male offspring were significantly hyperactive. This also eliminated the sex difference typically seen in this test. This effect persisted into adulthood. In the attention task, males exposed to nicotine during gestation showed a significant percent hit impairment. BaP reversed this effect. No significant effects were seen with percent correct rejection. These data show that both nicotine and BaP cause persisting sex‐selective behavioral effects that persist into adulthood.

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Toxicity study in juvenile rats with the α4β2 nicotinic acetylcholine receptor partial agonist CP-601,927

Campion

Hurtt

Chatman

et al. 2011

Birth Defects Research Part B: Developmental and Reproductive T

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Treatment-related findings included the death of 2 males receiving 3 mg/kg CP-601,927, and transient reductions in body weight for both males and females during the third week of dosing which quickly recovered to control levels. The only treatment-related alteration in behavior was decreased motor activity, which occurred only in females at the highest dose tested. CP-601,927 had no effect on acoustic startle response, learning and memory, sexual maturation, reproductive capacity, or general toxicity endpoints.

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An animal model of adolescent nicotine exposure: effects on gene expression and macromolecular constituents in rat brain regions

Cited by 182 publications

References 58 publications

Does Prenatal Nicotine Exposure Sensitize the Brain to Nicotine-Induced Neurotoxicity in Adolescence?

Does Prenatal Nicotine Exposure Sensitize the Brain to Nicotine-Induced Neurotoxicity in Adolescence?

Gestational exposure to nicotine and/or benzo[a]pyrene causes long‐lasting neurobehavioral consequences

Toxicity study in juvenile rats with the α4β2 nicotinic acetylcholine receptor partial agonist CP-601,927

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