Methamphetamine (METH) causes reactive gliosis in vitro: Attenuation by the ADP-ribosylation (ADPR) inhibitor, benzamide

We examined the effects of methamphetamine (METH) in an in vitro model of rat fetal mesencephalic cells. METH causes loss of dopamine (DA) cells and neuronal process degeneration. In addition, the drug causes an increase in reactive gliosis as shown by the number of cells that stain for and by the intensity of staining with a glial fibrillary acidic protein (GFAP) antibody. Co-incubation of METH-treated cells with benzamide, which is a known inhibitor of ADP-ribosylation (ADPR), attenuated METH effects on both DA and glial cells. However, the effects of benzamide were somewhat more prominent on the glial cells. These results suggest that ADP-ribosylation may play a very important role in the development of reactive gliosis after the administration of neurotoxic agents.