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. 2010 Mar 23;160(2):233–245. doi: 10.1111/j.1476-5381.2010.00663.x

Figure 3.

Figure 3

Effect of LA on MDMA-induced dopaminergic deficits, mitochondrial complex I inhibition and ROS production. LA (100 mg·kg−1 i.p.) or vehicle were given twice daily for 2 days, and MDMA (10, 20, 30 mg·kg−1 i.p. 2 h apart) was given 30 min after the fourth administration of LA or vehicle. (A) Striatal dopamine, DOPAC and HVA levels of mice 7 days after MDMA given alone or in combination with LA. Results shown as means ± SEM in pg·mg−1 wet tissue (n= 8–10). (B) Effect of LA on MDMA-induced acute hyperthermia. Arrows denote administration of LA or MDMA (solid arrows). Mice temperatures were recorded at baseline (t=–30 min) and 1 h after every injection of MDMA up to 7 h. Values are means ± SEM (n= 8–12 mice per group). (C) Complex I activity measured in the striata of mice 3 h after treatments. Results shown as means ± SEM (n= 8–12). (D) Effect of LA on MDMA-induced O2•− production. O2•− radicals were measured in animals treated with saline (control) or MDMA alone or in combination with LA. Note that LA decreased the ethidium signal evoked by MDMA. Results shown as means ± SEM (n= 3–4). In all panels: *P < 0.05, **P < 0.01 or ***P < 0.001 versus control group; †P < 0.01, different from MDMA-treated animals. One-way anova followed by Newman–Keuls test. DOPAC, 3,4-dihydroxyphenylacetic acid; HVA, homovanillic acid; LA, α-lipoic acid; MDMA, 3,4-methylenedioxymethamphetamine; ROS, reactive oxygen species.