MovDisordV3, Main, Exploration, bibRecord, 004430

In utero bacterial endotoxin exposure causes loss of tyrosine hydroxylase neurons in the postnatal rat midbrain

Identifieur interne : 004430 ( Main/Exploration ); précédent : 004429; suivant : 004431

In utero bacterial endotoxin exposure causes loss of tyrosine hydroxylase neurons in the postnatal rat midbrain

Auteurs : Zaodung Ling [États-Unis] ; Dave A. Gayle [États-Unis] ; Shang Yong Ma [États-Unis] ; Jack W. Lipton [États-Unis] ; Chong Wai Tong [États-Unis] ; Jau-Shyong Hong [États-Unis] ; Paul M. Carvey [États-Unis]

Source :

Movement Disorders [ 0885-3185 ] ; 2002-01.

RBID : ISTEX:28724E527A71F43C188A67EF039C112D4836FCC1

English descriptors

KwdEn :
- Animals, Animals, Newborn, Corpus Striatum (immunology), Corpus Striatum (metabolism), Dopamine (metabolism), Endotoxins (metabolism), Female, Fetal Diseases (immunology), Fetal Diseases (metabolism), Gestational Age, IL‐1β, Immunohistochemistry, Interleukin-1 (immunology), Mesencephalon (immunology), Mesencephalon (metabolism), Parkinson Disease (immunology), Parkinson Disease (metabolism), Parkinson's disease, Pregnancy, Prenatal Exposure Delayed Effects, Rats, Rats, Sprague-Dawley, Risk Factors, TNF‐α, Tumor Necrosis Factor-alpha (immunology), Tyrosine 3-Monooxygenase (deficiency), cytokines, dopamine, prenatal infection, risk factors for Parkinson's disease.
MESH :
- chemical , deficiency : Tyrosine 3-Monooxygenase.
- chemical , immunology : Interleukin-1, Tumor Necrosis Factor-alpha.
- chemical , metabolism : Dopamine, Endotoxins.
- immunology : Corpus Striatum, Fetal Diseases, Mesencephalon, Parkinson Disease.
- metabolism : Corpus Striatum, Fetal Diseases, Mesencephalon, Parkinson Disease.
- Animals, Animals, Newborn, Female, Gestational Age, Immunohistochemistry, Pregnancy, Prenatal Exposure Delayed Effects, Rats, Rats, Sprague-Dawley, Risk Factors.

Abstract

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 α (TNF‐α) kills DA neurons and is elevated in the brains of patients with Parkinson's disease (PD). LPS is a potent inducer of TNF‐α, 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‐α 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‐α (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. © 2001 Movement Disorder Society.

Url:

https://api.istex.fr/document/28724E527A71F43C188A67EF039C112D4836FCC1/fulltext/pdf

DOI: 10.1002/mds.10078

Affiliations:

Le document en format XML

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<author><name sortKey="Lipton, Jack W" sort="Lipton, Jack W" uniqKey="Lipton J" first="Jack W." last="Lipton">Jack W. Lipton</name>
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<term>Corpus Striatum (metabolism)</term>
<term>Dopamine (metabolism)</term>
<term>Endotoxins (metabolism)</term>
<term>Female</term>
<term>Fetal Diseases (immunology)</term>
<term>Fetal Diseases (metabolism)</term>
<term>Gestational Age</term>
<term>IL‐1β</term>
<term>Immunohistochemistry</term>
<term>Interleukin-1 (immunology)</term>
<term>Mesencephalon (immunology)</term>
<term>Mesencephalon (metabolism)</term>
<term>Parkinson Disease (immunology)</term>
<term>Parkinson Disease (metabolism)</term>
<term>Parkinson's disease</term>
<term>Pregnancy</term>
<term>Prenatal Exposure Delayed Effects</term>
<term>Rats</term>
<term>Rats, Sprague-Dawley</term>
<term>Risk Factors</term>
<term>TNF‐α</term>
<term>Tumor Necrosis Factor-alpha (immunology)</term>
<term>Tyrosine 3-Monooxygenase (deficiency)</term>
<term>cytokines</term>
<term>dopamine</term>
<term>prenatal infection</term>
<term>risk factors for Parkinson's disease</term>
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<term>Fetal Diseases</term>
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<front><div type="abstract" xml:lang="en">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 α (TNF‐α) kills DA neurons and is elevated in the brains of patients with Parkinson's disease (PD). LPS is a potent inducer of TNF‐α, 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‐α 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‐α (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. © 2001 Movement Disorder Society.</div>
</front>
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<tree><country name="États-Unis"><region name="Illinois"><name sortKey="Ling, Zaodung" sort="Ling, Zaodung" uniqKey="Ling Z" first="Zaodung" last="Ling">Zaodung Ling</name>
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<name sortKey="Carvey, Paul M" sort="Carvey, Paul M" uniqKey="Carvey P" first="Paul M." last="Carvey">Paul M. Carvey</name>
<name sortKey="Carvey, Paul M" sort="Carvey, Paul M" uniqKey="Carvey P" first="Paul M." last="Carvey">Paul M. Carvey</name>
<name sortKey="Gayle, Dave A" sort="Gayle, Dave A" uniqKey="Gayle D" first="Dave A." last="Gayle">Dave A. Gayle</name>
<name sortKey="Gayle, Dave A" sort="Gayle, Dave A" uniqKey="Gayle D" first="Dave A." last="Gayle">Dave A. Gayle</name>
<name sortKey="Hong, Jau Hyong" sort="Hong, Jau Hyong" uniqKey="Hong J" first="Jau-Shyong" last="Hong">Jau-Shyong Hong</name>
<name sortKey="Ling, Zaodung" sort="Ling, Zaodung" uniqKey="Ling Z" first="Zaodung" last="Ling">Zaodung Ling</name>
<name sortKey="Lipton, Jack W" sort="Lipton, Jack W" uniqKey="Lipton J" first="Jack W." last="Lipton">Jack W. Lipton</name>
<name sortKey="Lipton, Jack W" sort="Lipton, Jack W" uniqKey="Lipton J" first="Jack W." last="Lipton">Jack W. Lipton</name>
<name sortKey="Lipton, Jack W" sort="Lipton, Jack W" uniqKey="Lipton J" first="Jack W." last="Lipton">Jack W. Lipton</name>
<name sortKey="Ma, Shang Yong" sort="Ma, Shang Yong" uniqKey="Ma S" first="Shang Yong" last="Ma">Shang Yong Ma</name>
<name sortKey="Tong, Chong Wai" sort="Tong, Chong Wai" uniqKey="Tong C" first="Chong Wai" last="Tong">Chong Wai Tong</name>
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Movement Disorders (revue)

In utero bacterial endotoxin exposure causes loss of tyrosine hydroxylase neurons in the postnatal rat midbrain

In utero bacterial endotoxin exposure causes loss of tyrosine hydroxylase neurons in the postnatal rat midbrain

Source :

English descriptors

Abstract

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Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

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	Movement Disorders (revue)
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