Perinatal manganese exposure: Behavioral, neurochemical, and histopathological effects in the rat

Manganese chloride (Mn) was dissolved in the drinking water (0,2, or 10 mg/ml) of dams and their litters from conception until postnatal day (PND) 30. Parturition was uneventful in the Mn-exposed rats and no physical abnormalities were observed. The rats exposed to 10 mg/ml Mn showed a 2.5-fold incr...

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Published in:Neurotoxicology and teratology 1997, Vol.19 (1), p.17-25
Main Authors: Pappas, B.A., Zhang, D., Davidson, C.M., Crowder, T., Park, G.A.S., Fortin, T.
Format: Article
Language:English
Subjects:
Acetylcholine cortex
Analysis of Variance
Animals
Animals, Newborn
Biogenic Monoamines - metabolism
Biological and medical sciences
Brain - drug effects
Brain - pathology
Brain - physiopathology
Cerebral Cortex - drug effects
Chemical and industrial products toxicology. Toxic occupational diseases
Choline O-Acetyltransferase - metabolism
Female
Glial Fibrillary Acidic Protein - analysis
Male
Manganese Poisoning
Maze Learning - drug effects
Medical sciences
Metals and various inorganic compounds
Monoamines
Motor Activity - drug effects
Perinatal manganese
Pregnancy
Prenatal Exposure Delayed Effects
Rats
Rats, Sprague-Dawley
Spatial learning
Toxicology
Tyrosine 3-Monooxygenase - analysis
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Summary:Manganese chloride (Mn) was dissolved in the drinking water (0,2, or 10 mg/ml) of dams and their litters from conception until postnatal day (PND) 30. Parturition was uneventful in the Mn-exposed rats and no physical abnormalities were observed. The rats exposed to 10 mg/ml Mn showed a 2.5-fold increase in cortical Mn levels. Their weight gain was attenuated from PND 9–24 and they were hyperactive at PND 17. Neither the 2 nor the 10 mg/ml Mn-exposed groups differed from the controls on the elevated plus apparatus or on the Morris water maze and the radial arm maze. Brain monoamine levels and choline acetyltransferase activity were unaffected. Tyrosine hydroxylase immunohistochemistry showed that dopamine cells of the substantia nigra were intact. Glial fibrillary acidic protein immunoreactivity was not increased in cortex, caudate, and hippocampus. However, both the low- and high-dose Mn-exposed groups showing thinning of the cerebral cortex. This could have resulted from perinatal malnutrition or from a direct effect of Mn on cortical development.
ISSN:0892-0362
1872-9738
DOI:10.1016/S0892-0362(96)00185-7