β-Amyloid 25–35 Suppresses the Secretory Activity of the Dopaminergic System in the Rat Brain

Abstract

Dysfunction of the dopaminergic system of the brain may underlie a number of the clinical manifestations of Alzheimer’s disease. Published data provide evidence that impairments to the normal metabolism of β-amyloid may be the cause of such dysfunction. Experimental increases in β-amyloid levels in the brains of animals lead to decreases in the extracellular dopamine levels and its long-term (tonic) changes in the dorsal ventral striatum. The aim of the present work was to study the effects of β-amyloid on short-term (phasic) changes in dopamine secretion. Aggregated β-amyloid (25–35) solution or physiological saline was administered into the ventricular system of the brains of urethane-anesthetized rats. Dopamine release induced by electrical stimulation was recorded before administration and 10, 30, and 60 min after administration by fast-scan cyclic voltammetry. Dopamine release in the dorsomedial striatum was decreased during the first hour after β-amyloid administration. No statistically significant changes in the core and shell of the nucleus accumbens were seen.