AP-1 DNA-binding activation by methamphetamine involves oxidative stress.

P Sheng, X B Wang, B Ladenheim, C Epstein, J L Cadet
Author Information
  1. P Sheng: Section of Molecular Neuropsychiatry, Intramural Research Program, NIH/NIDA, Baltimore, Maryland 21224, USA.

Abstract

Methamphetamine (METH) caused dose-dependent increases in AP-1 DNA-binding activity in both nontransgenic (Non-Tg) and CuZn-SOD transgenic (SOD-Tg) mice. However, the increases in SOD-Tg mice were less prominent than those observed in Non-Tg animals. The time-course of METH-induced AP-1 changes was similar in both strains of mice. AP-1 binding activity showed an initial increase at 1 h, peaked at 3 h, and then gradually declined. AP-1 binding activity was back to normal by the 72-h time point. Regional analyses of METH effects revealed increases in the caudate putamen and cerebellum, with the striatum showing relatively higher METH-induced AP-1 DNA-binding activation. These regional effects were also attenuated in the SOD-Tg mice. These data indicate that METH-induced stimulation of AP-1 DNA-binding depends on cellular redox status. These results are consistent with in vitro studies that have reported that several transcription factors are regulated through redox mechanisms.

MeSH Term

Animals
Brain Chemistry
Central Nervous System Stimulants
DNA
Electrophoresis, Polyacrylamide Gel
Humans
Kinetics
Methamphetamine
Mice
Mice, Transgenic
Oxidative Stress
Superoxide Dismutase
Transcription Factor AP-1

Chemicals

Central Nervous System Stimulants
Transcription Factor AP-1
Methamphetamine
DNA
Superoxide Dismutase

Word Cloud

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