Modafinil treatment prevents methamphetamine-triggered effects on pro-apoptotic BAX and anti-apoptotic Bcl-2 protein expression in mice striatum [459.06/T19]

B. GONZALEZ; M. RAINERI; E. GARCIA-RILL; I. N. KRASNOVA; J. L. CADET; F. J. URBANO; V. BISAGNO

New Orleans, LA

Congreso; 2012 Society for Neuroscience Meeting; 2012

Society for Neuroscience

Methamphetamine (METH) intake can cause neurotoxic damage in human users and animals. METH toxic effects include terminal degeneration and pro-apoptotic effects. Previous results from our group had demonstrated that Modafinil (MOD), a psychostimulant drug used to treat sleep disorders, could protect against METH-induced striatal toxicity. To further evaluate the role of MOD in neuroprotection, we first studied the temporal profile of METH-induced toxicity in the striatum with the Amino-Cupric-Silver (A-Cu-Ag) technique (De Olmos et al.. 1994). This silver method stains with a high degree of selectivity all the components of degenerating neurons, including their cell bodies, dendritic arborization, as well as axonal processes and terminals. Female C57BL/6 mice were treated with a METH "binge" protocol (4x5mg/kg, i.p., 2h apart). This METH regimen was selected because it causes pronounced glial activation (see Raineri et al., SFN 2012). Post-mortem studies were done at 8, 16, 24, 48 hrs, and, 6 days after the last METH injection. METH-treated mice showed the highest degree of terminal degeneration at 16 and at 24 hours after the last METH injection (p