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Methamphetamine exposure affects α‐synuclein expression in the cortex
Author(s) -
GambleGeorge Joyonna Carrie,
Khoshbouei Habibeh
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.1005.2
Subject(s) - meth , methamphetamine , neurotoxicity , pharmacology , neuroprotection , addiction , chemistry , downregulation and upregulation , neuroscience , medicine , toxicity , psychology , biochemistry , gene , monomer , organic chemistry , acrylate , polymer
Methamphetamine (METH) is a highly addictive psychostimulant that is becoming a global public health problem. Previous studies have suggested that METH exposure is neurotoxic that may induce long‐lasting cognitive and motor impairments after cessation of drug use. α‐synuclein is implicated in neurodegenerative diseases. In this study, we propose that METH exposure affects the levels of α‐synuclein in the brain. Few studies have investigated the molecular mechanism of METH modulation of α‐synuclein in the brain. The present study sought to examine the effect of METH exposure via intraperitoneal injection (24 mg/kg/day) and an osmotic pump (1 mg/kg/hr) on α‐synuclein levels in the brains of juvenile C57BL/6J mice. We found that juvenile mice treated with METH for two weeks via osmotic pump showed an increase in α‐synuclein levels compared to saline‐treated control mice. This increase in α‐synuclein levels may be accountable for METH‐induced neurotoxicity. Since overexpression of α‐synuclein has been implicated in the dysregulation of DA homeostasis, we propose that METH‐induced α‐synuclein changes are dependent upon the pattern of METH administration. Currently, we are examining whether a correlation exists between alterations in α‐synuclein levels and additional molecular targets involved in DAergic homeostasis in the brain that are induced by METH exposure. This research was supported by NIH Grants U54NS041071, U54RR026140, DA026947, and DA021471.