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In utero bacterial endotoxin exposure causes loss of tyrosine hydroxylase
neurons in the postnatal rat midbrain
ZD Ling, DA Gayle, SY Ma, JW Lipton, CW Tong, JS Hong, PM Carvey
Movement Disorders 2002;17:116-124

In utero exposure to a common bacterial toxin reduces postnatal levels of
dopaminergic neurons in rats, according to this study. Lipopolysaccharide,
also known as endotoxin, is produced by Gram-negative bacteria. LPS is
known to enter the chorioamniotic environment, and is elevated in
bacterial vaginosis, a leading cause of premature delivery in humans.

Pregnant rats were injected with LPS at embryonic day 10.5. At postnatal
day 21, pup brains showed a 29% reduction in tyrosine hydroxylase
immunoreactive cells compared to controls, without a corresponding
reduction in the total number of brain neurons. Substantia nigra volume,
cell density, and cell body size were all reduced.

The authors conclude, "It is difficult not to draw parallels between
[bacterial vaginosis] in humans and prenatal LPS exposure in the rat…If
such a parallel were to exist, it would suggest that prenatal infections
such as BV occurring at the appropriate gestational age would result in
the birth of humans with fewer dopamine neurons," which may predispose
toward development of PD later in life.

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