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Prenatal lipopolysaccharide does not accelerate progressive dopamine neuron loss in the rat as a result of normal aging.
Exp Neurol. 2009 Apr; 216(2):312-20.EN

Abstract

We previously demonstrated that in utero exposure to the bacteriotoxin lipopolysaccharide (LPS) led to the birth of rat pups with fewer than normal dopamine (DA) neurons. These animals exhibited significant neuroinflammation in the nigrostriatal pathway creating the possibility that they could exhibit further, progressive DA neuron loss over their lives. To study this possibility, we injected gravid female rats i.p. at 10,000 endotoxin units (EUs) of LPS per kg or saline at embryonic (E) day 10.5 and assigned pups to sacrifice groups at 4, 14 and 17 months such that littermates were sacrificed at each end point. The effects of prenatal LPS on DA cell counts and striatal DA were significantly reduced relative to controls whereas DA activity and numbers of activated microglia (OX-6ir cell) were statistically increased. However, the progressive DA neuron loss was parallel to that of the controls suggesting that prenatal LPS does not produce an accelerated rate of DA neuron loss. Interestingly, locomotor activity was increased after 3 months in animals exposed to LPS prenatally, but by 16 months, was significantly reduced relative to controls. Additionally, animals exposed to LPS prenatally exhibited Lewy body-like inclusions that were first seen in 14 month old animals. These data broadly support previous studies demonstrating that prenatal exposure to LPS, as frequently occurs in humans as part of Bacterial Vaginosis, leads to the birth of animals with fewer than normal DA neurons. The progressive DA neuron loss seen in these animals is, however, primarily a result of normal aging.

Authors+Show Affiliations

Department of Pharmacology, Rush University Medical Center, Cohn Research Building, Suite 406, 1735 W. Harrison St., Chicago, IL 60612, USA. lingzdl@yahoo.comNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.

Language

eng

PubMed ID

19133261

Citation

Ling, Zaodung, et al. "Prenatal Lipopolysaccharide Does Not Accelerate Progressive Dopamine Neuron Loss in the Rat as a Result of Normal Aging." Experimental Neurology, vol. 216, no. 2, 2009, pp. 312-20.
Ling Z, Zhu Y, Tong CW, et al. Prenatal lipopolysaccharide does not accelerate progressive dopamine neuron loss in the rat as a result of normal aging. Exp Neurol. 2009;216(2):312-20.
Ling, Z., Zhu, Y., Tong, C. W., Snyder, J. A., Lipton, J. W., & Carvey, P. M. (2009). Prenatal lipopolysaccharide does not accelerate progressive dopamine neuron loss in the rat as a result of normal aging. Experimental Neurology, 216(2), 312-20. https://doi.org/10.1016/j.expneurol.2008.12.004
Ling Z, et al. Prenatal Lipopolysaccharide Does Not Accelerate Progressive Dopamine Neuron Loss in the Rat as a Result of Normal Aging. Exp Neurol. 2009;216(2):312-20. PubMed PMID: 19133261.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Prenatal lipopolysaccharide does not accelerate progressive dopamine neuron loss in the rat as a result of normal aging. AU - Ling,Zaodung, AU - Zhu,Yuangui, AU - Tong,Chong Wai, AU - Snyder,Joshua A, AU - Lipton,Jack W, AU - Carvey,Paul M, Y1 - 2008/12/16/ PY - 2008/08/30/received PY - 2008/11/29/revised PY - 2008/12/04/accepted PY - 2009/1/10/entrez PY - 2009/1/10/pubmed PY - 2009/4/16/medline SP - 312 EP - 20 JF - Experimental neurology JO - Exp Neurol VL - 216 IS - 2 N2 - We previously demonstrated that in utero exposure to the bacteriotoxin lipopolysaccharide (LPS) led to the birth of rat pups with fewer than normal dopamine (DA) neurons. These animals exhibited significant neuroinflammation in the nigrostriatal pathway creating the possibility that they could exhibit further, progressive DA neuron loss over their lives. To study this possibility, we injected gravid female rats i.p. at 10,000 endotoxin units (EUs) of LPS per kg or saline at embryonic (E) day 10.5 and assigned pups to sacrifice groups at 4, 14 and 17 months such that littermates were sacrificed at each end point. The effects of prenatal LPS on DA cell counts and striatal DA were significantly reduced relative to controls whereas DA activity and numbers of activated microglia (OX-6ir cell) were statistically increased. However, the progressive DA neuron loss was parallel to that of the controls suggesting that prenatal LPS does not produce an accelerated rate of DA neuron loss. Interestingly, locomotor activity was increased after 3 months in animals exposed to LPS prenatally, but by 16 months, was significantly reduced relative to controls. Additionally, animals exposed to LPS prenatally exhibited Lewy body-like inclusions that were first seen in 14 month old animals. These data broadly support previous studies demonstrating that prenatal exposure to LPS, as frequently occurs in humans as part of Bacterial Vaginosis, leads to the birth of animals with fewer than normal DA neurons. The progressive DA neuron loss seen in these animals is, however, primarily a result of normal aging. SN - 1090-2430 UR - https://www.unboundmedicine.com/medline/citation/19133261/Prenatal_lipopolysaccharide_does_not_accelerate_progressive_dopamine_neuron_loss_in_the_rat_as_a_result_of_normal_aging_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0014-4886(08)00472-X DB - PRIME DP - Unbound Medicine ER -