Dopaminergic dysfunction is a part of Alzheimer's disease pathology. The brain accumulation of amyloid-β of toxic form is a key link of the pathology, which, according to the literature, is also true for dopaminergic dysfunction. An increase in the amyloid-β level in the brain changes the maximum of the evoked dopamine release in the dorsal and ventral parts of the striatum of the experimental animals. Theoretically, this may be due to the change in the intensity of dopamine release from the nerve terminals or its reuptake. However, it has not been studied. To fill this gap, we examined the amyloid-β induced changes in the kinetics of the evoked dopamine release in the dorsal striatum and the nucleus accumbens core and shell. Amyloid-β solution (fragments 25-35) was injected into the ventricular system of the anesthetized male Wistar rats. Before and after injection, electrically evoked dopamine kinetics was registered with fast-scan cyclic voltammetry. The results had shown that the amount of dopamine release decreases in the dorsal striatum and increases in the nucleus accumbens shell. No changes were found in the intensity of dopamine reuptake.
Keywords: Alzheimer’s disease; Amyloid-β; Dopamine kinetics; Fast-scan cyclic voltammetry; Nucleus accumbens; Striatum.
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