Document Detail


Postnatal nicotine and/or intermittent hypercapnic hypoxia effects on apoptotic markers in the developing piglet brainstem medulla.
MedLine Citation:
PMID:  16905268     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The most important risk factors currently identified for the sudden infant death syndrome (SIDS) are prone sleeping and cigarette smoke exposure. In this study, we investigated the neuropathological sequelae of these risk factors by exposing piglets to intermittent hypercapnic-hypoxia (IHH) and/or nicotine (nic) in the early postnatal period. Our hypothesis was that either nic or IHH exposure could increase neuronal cell death, and that combined exposure (nic+IHH) would be additive. Four exposure patterns were studied: controls (n=14), IHH (n=10), nic (n=14), and nic+IHH (n=14). All groups had equal gender ratios. Nic exposure via an implanted osmotic minipump commenced within 48 h of birth and continued until age 13-14 days when animals were killed and brains collected. A total of 48 min of hypercapnic-hypoxia was delivered on the day immediately prior to killing in a pattern comprising 6 min of HH (8% O(2), 7% CO(2), balance N(2)) alternating with 6 min of air. Immunohistochemistry was performed to identify neurons positive for active caspase-3 and DNA fragmentation (terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling, TUNEL) in seven nuclei of the caudal medulla. Staining quantification showed that: 1. IHH induced neuronal death (increased both TUNEL and casapse-3) in more brainstem nuclei than nicotine. 2. Females were more severely affected by IHH than males. 3. Where IHH and nicotine were combined, TUNEL expression was approximately 5% less than IHH alone, but changes in caspase-3 were variable. We conclude that acute exposure to IHH in the postnatal period is more neurotoxic than exposure to nicotine alone. Combined exposure to IHH and nicotine produced variable responses with some results suggesting that nicotine can be neuroprotective. These results indicate that environmental insults attributable to prone sleeping can produce neurotoxic sequelae in SIDS, with some regional specificity in the response. However, no consistent relationship is evident when combining the two insults.
Authors:
R Machaalani; K A Waters
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't     Date:  2006-08-14
Journal Detail:
Title:  Neuroscience     Volume:  142     ISSN:  0306-4522     ISO Abbreviation:  Neuroscience     Publication Date:  2006 Sep 
Date Detail:
Created Date:  2006-09-18     Completed Date:  2006-12-20     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  7605074     Medline TA:  Neuroscience     Country:  United States    
Other Details:
Languages:  eng     Pagination:  107-17     Citation Subset:  IM    
Affiliation:
Department of Medicine, Room 206, Blackburn Building, D06, The University of Sydney, NSW 2006, Australia.
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MeSH Terms
Descriptor/Qualifier:
Analysis of Variance
Animals
Animals, Newborn
Apoptosis / drug effects*,  physiology
Caspase 3 / metabolism
Cell Count / methods
Female
Hypercapnia*
Immunohistochemistry / methods
In Situ Nick-End Labeling / methods
Male
Medulla Oblongata* / drug effects,  growth & development,  pathology
Nicotine / adverse effects*,  blood
Nicotinic Agonists / adverse effects*
Sex Factors
Swine
Swine, Miniature
Time Factors
Chemical
Reg. No./Substance:
0/Nicotinic Agonists; 54-11-5/Nicotine; EC 3.4.22.-/Caspase 3

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


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