Adolescent nicotine exposure causes persistent upregulation of nicotinic cholinergic receptors in rat brain regions

Trauth, Jennifer A; Seidler, Frederic J.; McCook, E.C.; Slotkin, Theodore A.

doi:10.1016/s0006-8993(99)01994-0

Cited by 210 publications

(184 citation statements)

References 54 publications

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“…Across all four age points, prenatal nicotine exposure did not elicit any significant reductions in body weight, but as in previous studies (Trauth et al, 1999(Trauth et al, , 2000b, adolescent nicotine reduced weights slightly during the treatment period (o10%, F 1,92 ¼ 7.7, po0.007), with a rapid return to normal upon discontinuing nicotine (data not shown). Prenatal nicotine exposure did not alter the subsequent ability of adolescent nicotine treatment to elicit the small decrement in body weight (no interaction of prenatal nicotine Â adolescent nicotine in ANOVA with the twofactor treatment design).…”

Section: Resultssupporting

confidence: 81%

“…The reasons underlying the sex-dependent effects of adolescent nicotine treatment have been outlined previously (Trauth et al, 1999(Trauth et al, , 2000bXu et al, 2003): neuronal cell turnover and plasticity, and hence the effects of agents that affect cell replication, differentiation and neurite outgrowth, are responsive to estrogen (Tanapat et al, 1999). Although we found significant interactions between prenatal and adolescent nicotine exposure, with only a few exceptions (eg total protein/DNA ratio in hippocampus on PN75) the alterations in these biomarkers, too, showed additive effects of the two treatments.…”

Section: Discussionmentioning

confidence: 99%

“…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%

“…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: 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: Resultssupporting

confidence: 81%

Section: Discussionmentioning

confidence: 99%

Section: Animals and Nicotine Infusionsmentioning

confidence: 99%

Section: Animals and Nicotine Infusionsmentioning

confidence: 99%

See 2 more Smart Citations

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

Abreu‐Villaça

Seidler

Slotkin

2004

Neuropsychopharmacol

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“…In this sense, the lack of an anxiety effect in males during the 5-day withdrawal due to nicotine or ethanol exposure was somewhat surprising. Regarding nicotine, behavioral alterations in males were expected since it has been already demonstrated that they show more persistent modifications in cholinergic systems, the primary targets of nicotine, after adolescent exposure (Trauth et al, 1999(Trauth et al, , 2000a. Conversely, our findings show that anxiety levels in females are clearly affected during short-term nicotine withdrawal, a result that is in line with previous findings in rats exposed to this drug during adolescence (Trauth et al, 2000b).…”

Section: Anxiogenic Effects During Withdrawalsupporting

confidence: 91%

Combined Exposure to Nicotine and Ethanol in Adolescent Mice Differentially Affects Anxiety Levels during Exposure, Short-Term, and Long-Term Withdrawal

Abreu‐Villaça

Nunes

Queiroz-Gomes

et al. 2007

Neuropsychopharmacol

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Smoking and consumption of alcoholic beverages are frequently associated during adolescence. This association could be explained by the cumulative behavioral effects of nicotine and ethanol, particularly those related to anxiety levels. However, despite epidemiological findings, there have been few animal studies of the basic neurobiology of the combined exposure in the adolescent brain. In the present work we assessed, through the use of the elevated plus maze, the short-and long-term anxiety effects of nicotine (NIC) and/or ethanol (ETOH) exposure during adolescence (from the 30th to the 45th postnatal day) in four groups of male and female C57BL/6 mice: (1) Concomitant NIC (nicotine free-base solution (50 mg/ml) in 2% saccharin to drink) and ETOH (ethanol solution (25%, 2 g/kg) i.p. injected every other day) exposure; (2) NIC exposure; (3) ETOH exposure; (4) Vehicle. C57BL/6 mice were selected, in spite of the fact that they present slower ethanol metabolism, because they readily consume nicotine in the concentration used in the present study. During exposure (45th postnatal day: PN45), our results indicated that ethanol was anxiolytic in adolescent mice and that nicotine reverted this effect. Short-term drug withdrawal (PN50) elicited sex-dependent effects: exposure to nicotine and/or ethanol was anxiogenic only for females. Although neither nicotine nor ethanol effects persisted up to 1 month postexposure (PN75), the coadministration elicited an anxiogenic response. In spite of the fact that generalizations based on the results from a single strain of mice are prone to shortcomings, our results suggest that the deficient response to the anxiolytic effects of ethanol in adolescents co-exposed to nicotine may drive higher ethanol consumption. Additionally, increased anxiety during long-term smoking and drinking withdrawal may facilitate relapse to drug use.

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Adolescence and Addiction

Lydon

Galván

Geier

2015

The Wiley Handbook on the Cognitive Neuroscience of Addiction

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Adolescent nicotine exposure causes persistent upregulation of nicotinic cholinergic receptors in rat brain regions

Cited by 210 publications

References 54 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?

Combined Exposure to Nicotine and Ethanol in Adolescent Mice Differentially Affects Anxiety Levels during Exposure, Short-Term, and Long-Term Withdrawal

Adolescence and Addiction

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