Fig. 5.

Endomorphin-1 given into the ventral tegmental area increases the extracellular dopamine in the posterior nucleus accumbens (A) and the increase of the extracellular dopamine in the posterior nucleus accumbens by endomorphin-1 was blocked by (−)-naloxone given into the ventral tegmental area (B). Groups of rats were microinjected with endomorphin-1 (1, 3 or 10 μg) or vehicle into the ventral tegmental area (A). In other groups of rats, (−)-naloxone (4 or 40 ng) or vehicle was co-microinjected into the ventral tegmental area with endomorphin-1 (10 μg). The perfusates from the microdialysis probe at the nucleus accumbens shell were collected every 15 min from 30 min before microinjection and continuously collected for another120 min (A) or 105 min (B) after microinjection. The perfusates were then analyzed their dopamine level. Each point represents the percent basal dopamine release and the vertical bar represents the S.E.M.; n = 3–9. Two-way ANOVA followed by Bonferroni post-test was used to test the difference between groups; (A) For the groups of the rats injected with different dose of endomorphin-1 versus vehicle F_{interaction (24, 189)} = 1.573, F_{treatment (3, 189)} = 4.44, F_{time (8, 189)} = 2.141, * P < 0.005. (B) For the group of rats injected with different dose of (−)-naloxone + endomorphin-1 versus vehicle + endomorphin-1, F_{interaction (18, 150)} = 3.338, F_{treatment (2, 150)} = 7.671, F_{time (9, 150)} = 11.17, * P < 0.01; only the data of the dopamine level after the 0 min time point were used for the statistic analysis; the group of rats microinjected with vehicle alone in (B) was not included in the statistic analysis.