Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
2004-7-21
pubmed:abstractText
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0893-133X
pubmed:author
pubmed:issnType
Print
pubmed:volume
29
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1440-50
pubmed:dateRevised
2011-5-18
pubmed:meshHeading
pubmed-meshheading:15039772-Aging, pubmed-meshheading:15039772-Animals, pubmed-meshheading:15039772-Body Weight, pubmed-meshheading:15039772-Brain, pubmed-meshheading:15039772-Cell Size, pubmed-meshheading:15039772-DNA, pubmed-meshheading:15039772-Female, pubmed-meshheading:15039772-Male, pubmed-meshheading:15039772-Membrane Proteins, pubmed-meshheading:15039772-Mesencephalon, pubmed-meshheading:15039772-Nerve Tissue Proteins, pubmed-meshheading:15039772-Neurites, pubmed-meshheading:15039772-Neuroglia, pubmed-meshheading:15039772-Neurons, pubmed-meshheading:15039772-Neurotoxicity Syndromes, pubmed-meshheading:15039772-Nicotine, pubmed-meshheading:15039772-Organ Size, pubmed-meshheading:15039772-Pregnancy, pubmed-meshheading:15039772-Prenatal Exposure Delayed Effects, pubmed-meshheading:15039772-Rats, pubmed-meshheading:15039772-Rats, Sprague-Dawley
pubmed:year
2004
pubmed:articleTitle
Does prenatal nicotine exposure sensitize the brain to nicotine-induced neurotoxicity in adolescence?
pubmed:affiliation
Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, NC 27710, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't