Harmaline-induced amnesia: Possible role of the amygdala dopaminergic system.

In this study, we examined the effect of bilateral intra-basolateral amygdala (intra-BLA) microinjections of dopamine receptor agents on amnesia induced by a β-carboline alkaloid, harmaline in mice. We used a step-down method to assess memory and then, hole-board method to assess exploratory behaviors. The results showed that pre-training intra-BLA injections of dopamine D1 receptor antagonist and agonist (SCH23390 (0.5μg/mouse) and SKF38393 (0.5μg/mouse), respectively) impaired memory acquisition. In contrast, pre-training intra-BLA injections of dopamine D2 receptor antagonist and agonist (sulpiride and quinpirole, respectively) have no significant effect on memory acquisition. Pre-training intra-peritoneal (i.p.) injection of harmaline (1mg/kg) decreased memory acquisition. However, co-administration of SCH 23390 (0.01μg/mouse) with different doses of harmaline did not alter amnesia. Conversely, pre-training intra-BLA injection of SKF38393 (0.1μg/mouse), sulpiride (0.25μg/mouse) or quinpirole (0.1μg/mouse) reversed harmaline (1mg/kg, i.p.)-induced amnesia. Furthermore, all above doses of drugs had no effect on locomotor activity. In conclusion, the dopamine D1 and D2 receptors of the BLA may be involved in the impairment of memory acquisition induced by harmaline.