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Cited by 89Nicotinic Acetylcholine Receptors StudyPrenatal Substance Exposure EffectsHearing, Cochlea, Tinnitus, Genetics

Neonatal nicotine exposure impairs nicotinic enhancement of central auditory processing and auditory learning in adult rats

Liang, Kevin, Poytress, Bonnie Sue, Chen, Yiling, Leslie, Frances M., Weinberger, Norman M., Metherate, Raju·2006·European Journal of Neuroscience
DOI 10.1111/j.1460-9568.2006.04945.x
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Abstract

Children of women who smoke cigarettes during pregnancy display cognitive deficits in the auditory-verbal domain. Clinical studies have implicated developmental exposure to nicotine, the main psychoactive ingredient of tobacco, as a probable cause of subsequent auditory deficits. To test for a causal link, we have developed an animal model to determine how neonatal nicotine exposure affects adult auditory function. In adult control rats, nicotine administered systemically (0.7 mg/kg, s.c.) enhanced the sensitivity to sound of neural responses recorded in primary auditory cortex. The effect was strongest in cortical layers 3 and 4, where there is a dense concentration of nicotinic acetylcholine receptors (nAChRs) that has been hypothesized to regulate thalamocortical inputs. In support of the hypothesis, microinjection into layer 4 of the nonspecific nAChR antagonist mecamylamine (10 microM) strongly reduced sound-evoked responses. In contrast to the effects of acute nicotine and mecamylamine in adult control animals, neither drug was as effective in adult animals that had been treated with 5 days of chronic nicotine exposure (CNE) shortly after birth. Neonatal CNE also impaired performance on an auditory-cued active avoidance task, while having little effect on basic auditory or motor functions. Thus, neonatal CNE impairs nicotinic regulation of cortical function, and auditory learning, in the adult. Our results provide evidence that developmental nicotine exposure is responsible for auditory-cognitive deficits in the offspring of women who smoke during pregnancy, and suggest a potential underlying mechanism, namely diminished function of cortical nAChRs.

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  • Nicotine exposure in rats during the second postnatal week disrupted auditory cortex glutamate synapses, linked to long-term auditory processing and learning deficits.

    “Exposure of rats to nicotine in the second postnatal week, corresponding to the third trimester of human fetal brain development,(147) disrupted the development of glutamate synapses in the auditory cortex, which has been associated with long-term deficits in auditory processing and learning.”

    From Developmental toxicity of nicotine: A transdisciplinary synthesis and implications for emerging tobacco products (2017) · cites this paper as [67]

  • Evidence from rodent studies supports the hypothesis that perinatal nicotine exposure via nAChRs alters the maturation of the thalamocortical neurons that relay sensory information from the thalamus to primary sensory cortex.

    “Evidence from rodent studies supports the hypothesis that perinatal nicotine exposure via nAChRs alters the maturation of the thalamocortical neurons that relay sensory information from the thalamus to primary sensory cortex [11, 29].”

    From Impaired auditory discrimination learning following perinatal nicotine exposure or β2 nicotinic acetylcholine receptor subunit deletion (2012) · cites this paper as [29]

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Authors
Liang, K., Poytress, B. S., Chen, Y., Leslie, F. M., Weinberger, N. M., & Metherate, R.
Affiliations
University of California, Irvine (US)
ORCID
Venue
European Journal of Neuroscience
Publisher
Wiley
Published
2006-08
Volume
24
Issue
3
Pages
857-866
ISSN
  • 0953-816X (ISSN-L)
  • 1460-9568
DOI
10.1111/j.1460-9568.2006.04945.x
OpenAlex
W2128869610
Cited by
89
References
78
Citations by year
2026: 1 · 2025: 1 · 2024: 2 · 2023: 5 · 2022: 4 · 2021: 1 · 2020: 4 · 2019: 4 · 2018: 8 · 2017: 7 · 2016: 2 · 2015: 2 · 2014: 3 · 2013: 4 · 2012: 7
FWCI
3.12
Type
journal article
Language
en
Open access
closed
Licence
onlinelibrary.wiley.com/termsAndConditions#vor (vor, 13 d)
Locations
  • European Journal of Neuroscience (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Centre National d’Etudes Spatiales
  • National Institute on Drug Abuse (DA-10612, DA-12929, DA 07318, R01DA010612, R01DA012929)
  • National Institute on Deafness and Other Communication Disorders (DC 02967, DC02398, DC-05592, R01DC005592)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nicotinic Acetylcholine Receptors Study
  • Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Prenatal Substance Exposure Effects
  • Life Sciences › Neuroscience › Sensory Systems › Hearing, Cochlea, Tinnitus, Genetics
Keywords
prenatal tobacco exposure, nicotinic acetylcholine receptors, primary auditory cortex, auditory learning, mecamylamine, thalamocortical input, chronic nicotine exposure, maternal smoking, animal models
MeSH terms
Acetylcholine, Animals, Animals, Newborn, Auditory Cortex, Auditory Pathways, Avoidance Learning, Cognition Disorders, Disease Models, Animal, Female, Geniculate Bodies, Language Development Disorders, Learning Disabilities, Male, Nicotine, Pregnancy, Prenatal Exposure Delayed Effects, Receptors, Nicotinic, Smoking, Rats, Sprague-Dawley, Nicotinic Agonists, Nicotinic Antagonists, Rats

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