Action and Interaction of Amyloid-β and Insulin on Dopamine Release and Reuptake in the Dorsal Lateral Striatum of Rats

Accumulation of amyloid-β (Aβ) in the brain is an importantlink in the pathogenesis of Alzheimer's disease. Experimental studiesshow that Aβ can cause dopaminergic dysfunction that is characteristicof this disease and, under Aβ influence, not only the decrease butalso the increase in phasic dopamine release is possible, dependingon the structure of the brain. We aimed to investigate whether Aβin a toxic form affects dopamine release or reuptake in the dorsallateral striatum and, if so, whether this influence is mediatedby the insulin signaling pathway. Aβ (fragment 25–35) and insulinsolutions were injected into the ventricular system of the anesthetizedmale Wistar rats. Within 10 min before and 30 min after the injection,electrically evoked dopamine elevations were registered with fast-scancyclic voltammetry every 5 min. Release and reuptake were assessedseparately by kinetic analysis. The results show that Aβ acts ondopamine release and reuptake in the dorsal lateral striatum inseveral ways. It modulates the effect of insulin on dopamine releaseand reuptake. In addition, Aβ increases dopamine release and basal levelsby acting separately from the insulin signaling pathway.