Source:http://linkedlifedata.com/resource/pubmed/id/11835448
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
1
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| pubmed:dateCreated |
2002-2-8
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| pubmed:abstractText |
We investigated whether in utero exposure to the Gram(-) bacteriotoxin lipopolysaccharide (LPS) induces dopamine (DA) neuron loss in rats. The proinflammatory cytokine tumor necrosis factor alpha (TNF-alpha) kills DA neurons and is elevated in the brains of patients with Parkinson's disease (PD). LPS is a potent inducer of TNF-alpha, and both are increased in the chorioamniotic environment of women who have bacterial vaginosis (BV) during pregnancy, suggesting that BV might interfere with the normal development of fetal DA neurons. Gravid female rats were injected intraperitoneally with either LPS or normal saline at embryonic day 10.5 and their pups were killed at postnatal day 21. The brains of the pups were assessed for DA and TNF-alpha levels and DA cell counts in the mesencephalon using tyrosine hydroxylase immunoreactive (THir) cells as a DA neuron marker. Prenatal LPS exposure significantly reduced striatal DA (29%) and increased DA activity (72%) as well as TNF-alpha (101%). Stereological cell counts in the mesencephalon were also significantly reduced (27%) by prenatal LPS exposure. Prenatal exposure to LPS, as might occur in humans with BV, produces a significant loss of THir cells in rats that is still present 33 days following a single injection of LPS. Since this cell loss is well past the normal phase of DA neuron apoptosis that occurs in early postnatal life, rats so exposed may have a permanent loss of DA neurons, suggesting that prenatal infections may represent risk factors for PD.
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| pubmed:grant | |
| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical | |
| pubmed:status |
MEDLINE
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| pubmed:month |
Jan
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| pubmed:issn |
0885-3185
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| pubmed:author | |
| pubmed:copyrightInfo |
Copyright 2001 Movement Disorder Society.
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| pubmed:issnType |
Print
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| pubmed:volume |
17
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
116-24
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| pubmed:dateRevised |
2007-11-14
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| pubmed:meshHeading |
pubmed-meshheading:11835448-Animals,
pubmed-meshheading:11835448-Animals, Newborn,
pubmed-meshheading:11835448-Corpus Striatum,
pubmed-meshheading:11835448-Dopamine,
pubmed-meshheading:11835448-Endotoxins,
pubmed-meshheading:11835448-Female,
pubmed-meshheading:11835448-Fetal Diseases,
pubmed-meshheading:11835448-Gestational Age,
pubmed-meshheading:11835448-Immunohistochemistry,
pubmed-meshheading:11835448-Interleukin-1,
pubmed-meshheading:11835448-Mesencephalon,
pubmed-meshheading:11835448-Parkinson Disease,
pubmed-meshheading:11835448-Pregnancy,
pubmed-meshheading:11835448-Prenatal Exposure Delayed Effects,
pubmed-meshheading:11835448-Rats,
pubmed-meshheading:11835448-Rats, Sprague-Dawley,
pubmed-meshheading:11835448-Risk Factors,
pubmed-meshheading:11835448-Tumor Necrosis Factor-alpha,
pubmed-meshheading:11835448-Tyrosine 3-Monooxygenase
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| pubmed:year |
2002
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| pubmed:articleTitle |
In utero bacterial endotoxin exposure causes loss of tyrosine hydroxylase neurons in the postnatal rat midbrain.
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| pubmed:affiliation |
Department of Pharmacology, Rush-Presbyterian-St. Luke's Medical Center, Chicago, Illinois, USA. zling@rush.edu
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| pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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