Journal
JOURNAL OF NEUROSCIENCE RESEARCH
Volume 70, Issue 1, Pages 82-89Publisher
WILEY-LISS
DOI: 10.1002/jnr.10370
Keywords
abused drugs; neurotoxicity; oxidative stress; AP-1; CREB
Categories
Funding
- NIEHS NIH HHS [P42 ES007380] Funding Source: Medline
- NIMH NIH HHS [MH63022] Funding Source: Medline
- NINDS NIH HHS [NS39254] Funding Source: Medline
Ask authors/readers for more resources
Cellular oxidative stress and alterations in redox status can be implicated in methamphetamine (METH)-induced neurotoxicity. To elucidate the molecular signaling pathways of METH-induced neurotoxicity, we investigated the effects of a single intraperitoneal injection of METH (1.0, 10, or 20 mg/kg) on DNA-binding activity of specific redox-sensitive transcription factors in mouse brain. Transcription factors studied included activator protein-1 (AP-1), nuclear factor-kappaB (NF-kappaB), cAMP-responsive element-binding protein (CREB), SP-1, and signal transducers and activators of transcription (STAT1 and STAT3). Significant and dose-dependent inductions of AP-1 and CREB DNA-binding activities were observed in four different regions (striatum, frontal cortex, hippocampus, and cerebellum) isolated from the brains of mice injected with METH. However, injections with METH did not affect DNA binding activities of NF-kappaB, SP-1, STAT1, and STAT3. These results suggest that METH-induced oxidative stress may trigger the molecular signaling pathways via specific and selective activation of AP-1 and CREB. (C) 2002 Wiley-Liss, Inc. (C) 2002 Wiley-Liss, Inc.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available