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

Full 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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Author information

Author/s: Liang, Kevin (K); Poytress, Bonnie Sue (BS); Chen, Yiling (Y); Leslie, Frances M (FM); Weinberger, Norman M (NM); Metherate, Raju (R);

Affiliation: Department of Neurobiology and Behavior, University of California, Irvine, CA 92697, USA.

Grants: DA07318 (Agency:NIDA NIH HHS) ; DA10612 (Agency:NIDA NIH HHS) ; DA12929 (Agency:NIDA NIH HHS) ; DC02398 (Agency:NIDCD NIH HHS) ; DC02967 (Agency:NIDCD NIH HHS) ; DC05592 (Agency:NIDCD NIH HHS)

Journal and publication information

Publication Type: Journal Article; Research Support, N.I.H., Extramural

Journal: The European journal of neuroscience (Eur J Neurosci), published in France. (Language: eng)

Reference: 2006-Aug; vol 24 (issue 3) : pp 857-66

Dates: Created 2006/08/25; Completed 2006/11/01; Revised 2007/11/14;

PMID: 16848798, status: MEDLINE (last retrieval date: 12/26/2008)

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MeSH headings (categories)

This article was linked to the MESH Headings shown below.

Acetylcholine - metabolism
Animals
Animals, Newborn
Auditory Cortex - drug effects; growth & development; physiopathology
Auditory Pathways - drug effects; growth & development; physiopathology
Avoidance Learning - drug effects; physiology
Cognition Disorders - chemically induced; physiopathology
Disease Models, Animal
Female
Geniculate Bodies - drug effects; growth & development; physiopathology
Language Development Disorders - chemically induced; physiopathology

Learning Disorders - chemically induced; physiopathology
Male
Nicotine - adverse effects
Nicotinic Agonists - adverse effects
Nicotinic Antagonists - pharmacology
Pregnancy
Prenatal Exposure Delayed Effects - physiopathology
Rats
Rats, Sprague-Dawley
Receptors, Nicotinic - drug effects; metabolism
Smoking - adverse effects

Associated Chemicals: Nicotinic Agonists (0) ; Nicotinic Antagonists (0) ; Receptors, Nicotinic (0) ; Acetylcholine (51-84-3) ; Nicotine (54-11-5)

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