Prenatal nicotine exposure and cognitive performance in rats
Abstract
In humans and animal models there is evidence that prenatal nicotine exposure causes lasting deficits in cognitive performance. The current study examined the cognitive effects of prenatal exposure of rats to 2 mg/kg/day of nicotine. This dose did not cause significant deficits in maternal weight gain, offspring litter size, or pup weight. The control offspring showed the normal ontogeny of spontaneous alternation from near chance (50%) performance to 80%-85% alternation. In contrast, the nicotine-exposed rats had the opposite progression with abnormally high alternation on days 22-30 and abnormally low alternation on days 35-52. Acquisition of choice accuracy performance on the radial-arm maze (RAM) was not altered in a major way by nicotine exposure. Minor nicotine-induced changes in choice accuracy were seen during the initial trials of acquisition. The nicotine exposed female offspring had a significantly longer response duration. Prenatal nicotine exposure did significantly alter the effects of subsequent drug challenges on choice accuracy performance. The nicotine-exposed male offspring were significantly more responsive to the amnestic effects of the nicotinic antagonist mecamylamine. In a subsequent challenge, the effects of the beta-adrenergic antagonist propranolol were examined. A significant dose-related impairment in choice accuracy was seen in the control rats. In contrast, the nicotine-exposed rats did not show any significant response to propranolol. This decreased responsiveness to adrenergic challenge parallels the reduction in adrenergic response to nicotine challenge we previously found in littermates to the rats of the current study. Prenatal nicotine exposure causes subtle alterations in cognitive performance that can be magnified by challenges of nicotinic and adrenergic systems.
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Animal studies of prenatal nicotine exposure and cognitive development are more consistent, suggesting global learning and memory impairments.
“there is greater consistency among animal studies examining the effects of prenatal nicotine exposure on cognitive development, suggestive of global impairments in learning and memory.”
From Developmental toxicity of nicotine: A transdisciplinary synthesis and implications for emerging tobacco products (2017) · cites this paper as [184]
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- Authors
- Levin, E. D., Briggs, S. J., Christopher, N. C., & Rose, J. E.
- Affiliations
- Duke Medical Center (US)
- Duke University (US)
- Corresponding author
- Levin, Edward D.
- ORCID
- Levin, Edward D.
- Venue
- Neurotoxicology and Teratology
- Publisher
- Elsevier BV
- Published
- 1993-07
- Volume
- 15
- Issue
- 4
- Pages
- 251-260
- ISSN
- 0892-0362 (ISSN-L)
- OpenAlex
- W2025340326
- Cited by
- 130
- References
- 4
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 1 · 2023: 2 · 2022: 6 · 2021: 7 · 2020: 2 · 2019: 4 · 2018: 3 · 2017: 3 · 2016: 4 · 2015: 4 · 2014: 5 · 2013: 4 · 2012: 3
- FWCI
- 2.82
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neurotoxicology and Teratology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Prenatal Substance Exposure Effects
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nicotinic Acetylcholine Receptors Study
- Health Sciences › Medicine › Physiology › Smoking Behavior and Cessation
- Keywords
- prenatal nicotine exposure, cognitive performance, spontaneous alternation, radial maze, mecamylamine, propranolol, nicotinic acetylcholine receptors, adrenergic system, offspring behavior
- MeSH terms
- Animals, Birth Weight, Body Weight, Cognition, Dose-Response Relationship, Drug, Female, Infusions, Intravenous, Learning, Male, Mecamylamine, Memory, Nicotine, Pregnancy, Prenatal Exposure Delayed Effects, Propranolol, Weight Gain, Rats, Sprague-Dawley, Rats
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