Pan-Hou H, Suda Y, Ohe Y, Sumi M, Yoshioka M
Faculty of Pharmaceutical Sciences, Setsunan University, Osaka, Japan.
Brain Res. 1990 Jun 18;520(1-2):351-3. doi: 10.1016/0006-8993(90)91729-z.
Aspartame (L-aspartyl-L-phenylalanine methyl ester), an artificial low-calorie sweetener, was shown to dose-dependently inhibit L-[3H]glutamate binding to its N-methyl-D-aspartate-specific receptors. L-Aspartic acid, a major endogenous metabolite of aspartame, inhibited the binding more stronger than aspartame, while the other metabolites, L-phenylalanine and methanol, had no effect at the same concentration. Aspartame caused a significant change in the affinities of L-[3H]glutamate binding without altering the Vmax values of the binding, suggesting the inhibition is competitive. These in vitro findings suggested that aspartame may act directly on the N-methyl-D-aspartate-sensitive glutamate recognition sites in the brain synaptic membranes.
