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

•Pre-train infusion of SCH23390, SKF38393 and harmaline impaired memory acquisition.•Intra-BLA injection of sulpiride and quinpirole did not change memory acquisition.•Administration of SCH23390 did not alter amnesia induced by harmaline.•Infusion of SKF38393, sulpiride or quinpirole reversed amnesia caused by harmaline.•The dopaminergic system of amygdala may modulate harmaline-induced amnesia.

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 (0.5 μg/mouse) and SKF38393 (0.5 μg/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 (1 mg/kg) decreased memory acquisition. However, co-administration of SCH 23390 (0.01 μg/mouse) with different doses of harmaline did not alter amnesia. Conversely, pre-training intra-BLA injection of SKF38393 (0.1 μg/mouse), sulpiride (0.25 μg/mouse) or quinpirole (0.1 μg/mouse) reversed harmaline (1 mg/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.