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In PC12 Cells Neurotoxicity Induced by Methamphetamine Is Related to Proteasome Inhibition
Author(s) -
LAZZERI GLORIA,
LENZI PAOLA,
GESI MARCO,
FERRUCCI MICHELA,
FULCERI FEDERICA,
RUGGIERI STEFANO,
BRUNO VALERIA,
FORNAI FRANCESCO
Publication year - 2006
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1196/annals.1369.017
Subject(s) - methamphetamine , programmed cell death , neurotoxicity , intracellular , meth , viability assay , microbiology and biotechnology , cell , inclusion bodies , cell bodies , chemistry , neuroscience , proteasome , toxicity , apoptosis , autophagy , biology , pharmacology , biochemistry , central nervous system , monomer , organic chemistry , escherichia coli , acrylate , gene , polymer
Neurodegenerative disorders are featured by a variety of pathological hallmarks, and very often they are characterized by neuronal inclusions in specific brain nuclei. Occurrence of neuronal inclusions has been often related to the onset of cell death. Recent studies demonstrated that amphetamine derivatives produce intracellular inclusions, which are reminiscent of those occurring in degenerative disorders. In the present article, we analyzed the correlation between neuronal inclusions and cell death using methamphetamine (METH) in PC12 cell cultures. We found that the dose necessary to induce cell death is higher compared with that required to induce inclusions formation. Our results demonstrate a dissociation between formation of inclusion bodies and cell death suggesting that neuronal inclusions do not necessarily lead to cell death. The conclusions of the present article suggest that the onset of inclusion bodies represents a slight consequence of toxicity, which requires a prolonged cell viability to take place.