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Effect of Developmental Lead Exposure on the Expression of Hippocampal NMDA Receptor Subunit mRNA
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Tae Wan Kim, In Sung Chung, Jae Hoon Bae, Dong Hoon Shin, Mi Young Lee, Joon Sik Kim
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Korean Journal of Occupational and Environmental Medicine 2005;17(4):278-287. Published online December 31, 2005
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DOI: https://doi.org/10.35371/kjoem.2005.17.4.278
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 Abstract
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- OBJECTIVES
The purpose of the present study was to examine the differential effects of lead (Pb) exposure on the expression of specific NMDA receptor subunit mRNAs on the hippocampal cells depending on the neuronal developmental stage.
METHODS
Expression of the NR2A and NR2B subunits of the NMDA receptors mRNA on the hippocampal neurons was measured by in situ hybridization in the control and Pb treated groups. Pb-treated and NMDA cytotoxicity was assessed by morphological examination and LDH measurements.
RESULTS
Hippocampal NR2A subunit mRNA expression was gradually increased with increasing age, and was significantly decreased after Pb exposure. The expression of NR2B subunit mRNA was not changed during development in the rat hippocampus and the developmental effect of Pb exposure on NR2B expression was minimal. These results indicate that chronic Pb exposure may decrease the levels of NR2A-containing NMDA receptors and may thereby alter normal synaptic signal transmission. Pb or NMDA-induced cytotoxicity in vitro differed significantly between the immature and the mature hippocampal cells.
CONCLUSIONS
This study demonstrates that chronic Pb exposure during brain development alters the levels of specific NMDA receptor subunit mRNA in the rat hippocampus. These results suggest that chronic Pb exposure may attenuate the precise neuronal synaptic transmission through the differential alteration of the composition of the NMDA receptor subunit on the hippocampus depending on neuronal developmental stage.
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Apoptosis Induced by Manganese in Basal Ganglia Primary Neuronal Cell Culture: Morphological Findings
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Dong Hoon Shin, Sang Pyo Kim, Young Wook Jung, Jae Hoon Bae, Dae Kyu Song, Won Ki Baek
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Korean Journal of Occupational and Environmental Medicine 2000;12(1):41-47. Published online March 31, 2000
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DOI: https://doi.org/10.35371/kjoem.2000.12.1.41
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Abstract
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- OBJECTIVES
Manganese is cytotoxic to the central nervous system including basal ganglia.
Its toxic mechanism is related to oxidative stress, mediated by toxic free radicals but is specultives.
In the present study, we have investigated to manifest apoptosis in manganese-induced cytotoxicity in primary neuronal cell culture of rat basal ganglia.
METHOD
To detect apoptotic neuronal cells were stained by the terminal deoxynu-cleotide(TdT)-mediated dUTP nick end-labelling(TUNEL) method and apoptotic changes in nuclei of neurons were observed by electron microscopy.
RESULTS
We showed that TUNEL immunostain showed brownish signal in the nuclei of apoptotic cells and the proportions of apoptotic cells in Manganese treatment groups were more higher than controls. On transmission electron microscopy, there were chromatine condensation with margination toward nuclear membrane and condensation of cytoplasm in the treated with luM MnC1, for 48 hours in a basal ganglia neurons.
Apoptotic bodies were found and consisted of semilunar-like condensed nuclei with relatively intact cytoplasmic organelles.
CONCLUSIONS
Apoptosis appears to be one mechanism in the manganese-induced neuronal cell death.
Manganese intoxication is a convenient model for apoptosis study.
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KSOEM
