Abstract
We investigated whether the psychostimulant methamphetamine (METH) has a cytotoxic effect on oligodendrocytes and which cell-death pathways are involved in the cytotoxic process. METH caused concentration- and time-dependent cytotoxicity in rat oligodendrocyte cultures. METH induced apoptotic cell death and mRNA expression of pro-apoptotic proteins (bax and DP5), but not anti-apoptotic proteins (bcl-2 and bcl-XL). These results suggest that METH induces cytotoxicity in rat oligodendrocytes via the differential regulation of the expression of genes involved in the apoptotic process.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Animals
-
Apoptosis Regulatory Proteins
-
Apoptosis*
-
Cytotoxins / pharmacology*
-
Methamphetamine / pharmacology*
-
Neuropeptides / genetics
-
Oligodendroglia / drug effects*
-
Oligodendroglia / metabolism
-
Oligodendroglia / physiology*
-
Proto-Oncogene Proteins / genetics
-
Proto-Oncogene Proteins c-bcl-2 / genetics
-
RNA, Messenger / metabolism
-
Rats
-
Rats, Wistar
-
bcl-2-Associated X Protein
-
bcl-X Protein
Substances
-
Apoptosis Regulatory Proteins
-
Bax protein, rat
-
Bcl2l1 protein, rat
-
Cytotoxins
-
Hrk protein, rat
-
Neuropeptides
-
Proto-Oncogene Proteins
-
Proto-Oncogene Proteins c-bcl-2
-
RNA, Messenger
-
bcl-2-Associated X Protein
-
bcl-X Protein
-
Methamphetamine