Document Detail


Does prenatal nicotine exposure sensitize the brain to nicotine-induced neurotoxicity in adolescence?
MedLine Citation:
PMID:  15039772     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
Yael Abreu-Villaça; Frederic J Seidler; Theodore A Slotkin
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology     Volume:  29     ISSN:  0893-133X     ISO Abbreviation:  Neuropsychopharmacology     Publication Date:  2004 Aug 
Date Detail:
Created Date:  2004-07-21     Completed Date:  2004-09-08     Revised Date:  2011-05-18    
Medline Journal Info:
Nlm Unique ID:  8904907     Medline TA:  Neuropsychopharmacology     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1440-50     Citation Subset:  IM    
Affiliation:
Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, NC 27710, USA.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Aging / physiology
Animals
Body Weight / drug effects
Brain / drug effects*,  physiopathology
Cell Size
DNA / metabolism
Female
Male
Membrane Proteins / metabolism
Mesencephalon / drug effects,  metabolism
Nerve Tissue Proteins / metabolism
Neurites / drug effects,  pathology
Neuroglia / drug effects,  pathology
Neurons / drug effects,  pathology
Neurotoxicity Syndromes / physiopathology*
Nicotine / administration & dosage,  toxicity*
Organ Size / drug effects
Pregnancy
Prenatal Exposure Delayed Effects*
Rats
Rats, Sprague-Dawley
Chemical
Reg. No./Substance:
0/Membrane Proteins; 0/Nerve Tissue Proteins; 54-11-5/Nicotine; 9007-49-2/DNA

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Behavioral and neurochemical consequences of long-term intravenous self-administration of MDMA and i...
Next Document:  Simultaneous blockade of adenosine A2A and metabotropic glutamate mGlu5 receptors increase their eff...