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Temporal profiling of methamphetamine-induced changes in gene expression in the mouse brain: evidence from cDNA array
J L Cadet1, S Jayanthi, M T McCoy
1Molecular Neuropsychiatry Section, NIH/NIDA, Intramural Research Program, Baltimore, Maryland 21224, USA. jcadet@intra.nida.nih.gov
Synapse (New York, N.Y.)
|May 17, 2001
Summary
Methamphetamine (METH) causes neurodegeneration by affecting gene expression. Early changes involve transcription factors, followed by genes related to cell death and repair, highlighting a complex cellular response.
Area of Science:
- Neuroscience
- Toxicology
- Molecular Biology
Background:
- Methamphetamine (METH) is a neurotoxic drug of abuse.
- METH-induced neurotoxicity involves monoaminergic terminal destruction and apoptosis.
- Free radicals and transcription factors are implicated in METH neurotoxicity.
Purpose of the Study:
- To investigate the temporal gene expression patterns in the mouse cortex following METH administration.
- To identify molecular mechanisms underlying METH-induced neurodegeneration.
Main Methods:
- Utilized cDNA arrays to survey gene expression changes in mouse cortical tissue.
- Analyzed temporal profiles of gene expression patterns after METH treatment.
Main Results:
- Identified two distinct temporal gene expression patterns.
- Early pattern: Upregulation of transcription factors, including jun family members.
- Delayed pattern: Upregulation of genes involved in cell death, DNA repair, and trophic factors.
Conclusions:
- METH triggers a multigene response contributing to its neurotoxic effects.
- Neurodegeneration results from a balance between pro-apoptotic and anti-apoptotic mechanisms.
- Findings have clinical relevance for understanding METH abuser brain changes.