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. 2009 Dec 10;159(1):201–211. doi: 10.1111/j.1476-5381.2009.00522.x

Figure 5.

Figure 5

Effect of repeated cocaine (20 mg·kg−1, i.p. twice daily separated by 8 h for 3 days) finishing 4 days before on 3,4-methylenedioxymethamphetamine (MDMA) (20 mg·kg−1, i.p., two injections separated 3 h)-induced changes in extracellular (A) dopamine (DA), (B) DOPAC and (C) HVA concentration in striatum. MDMA increased extracellular levels of dopamine [F1,11= 37.8, P < 0.001] and decreased levels of DOPAC [F1,12= 79.05, P < 0.001] and HVA [F1,10= 3.61, P < 0.05] compared with saline-treated animals. Pretreatment of the animals with cocaine finishing 4 days before MDMA potentiated this increase in extracellular dopamine levels [F1,19= 7.53, P < 0.01], but did not modify levels of DOPAC [F1,18= 0.75, P= 0.36; n.s.] or HVA [F1,17= 0.20, P= 0.64, n.s.]. Data expressed as % of baseline values. Results represent mean ± SEM, n= 4 − 11; two-way anova. Basal dopamine concentrations were lower in mice pretreated with cocaine compared with saline-treated mice (bar graph). Different from saline-pretreated mice: *P < 0.05 (t-test). Basal DOPAC and HVA levels were similar between groups, for DOPAC (pg·µL−1): 182.0 ± 16.2 versus 185.0 ± 20.0 for saline- and cocaine-pretreated mice, respectively (P= 0.91, n.s., t-test) and for HVA (pg·µL−1): 117.7 ± 13.1 versus 118.8 ± 13.5 for saline- and cocaine-pretreated mice, respectively (P= 0.95, n.s., t-test).