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Methamphetamine‐induce neurotoxic effects in rat c6 glioma cell (LB620)
Author(s) -
Wiley Chantel
Publication year - 2014
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.28.1_supplement.lb620
Subject(s) - methamphetamine , viability assay , apoptosis , neurotoxicity , flow cytometry , programmed cell death , pharmacology , annexin , biology , microbiology and biotechnology , medicine , immunology , toxicity , biochemistry
PURPOSE: Methamphetamine (MA) is a potent, highly addictive central nervous system stimulant. It has been classified as a Schedule II drug, which makes it legally available, but only through a no refillable prescription. MA addiction has become a major public concern because its chronic abuse is associated with serious, yet fatal side effects such as memory loss, stroke, hyperthermia, and convulsions. These complex complications of the central nervous system may be related to a MA‐induced neurotoxic effect, which include damage to the dopamine system, activation of microglial and astrogial cells, and ultimately destruction of specific brain regions in humans. The present study seeks to investigate the cellular events associated with cytotoxic effects of MA in the Rat C6 glial cells. METHOD: Using the crystal violet assay to quantitate cell viability, methamphetamine at various concentrations (0.1 mM, 0.5 mM, 1 mM, 3 mM, and 5 mM) was exposed to the glial cells for 1, 24 and 48 hrs. To measure the morphological alterations after MA exposure, FITC Annexin V flow cytometry was used to distinguish cells that were in early and late stage of apoptosis. RESULTS: MA was found to have a dose and time dependent effect on cell viability. In addiction, the FITC Annein V Flow cytometry data revealed that as the concentrations increased more cells underwent apoptosis. These results revealed that MA not only cause a decrease in viability among C6 glioma cells, but is also the causes of the cellular demise was through the action of apoptosis. CONCLUSION: Further studies are underway to elucidate the mechanism by which MA induces apoptosis. The data generated from this study has provided some significant findings regarding the cellular mechanism of MA‐induced cytotoxicity in the Rat C6 glial cells. Moreover, our results can lead to potentially safe therapeutic treatments for neurodegenerative disorders that are associated with chronic drug use. Grant Funding Source : Research supported by NIMHD of the National Institutes of Health NIH under Award Number G12MD007582