Monosodium glutamate (MSG) is a widely used nutritional substance that potentially exhibits significant neuronal toxicity. The present study was undertaken to further investigate the links between obesity, voracity, and MSG toxicity, and to test the possibility of using a non competitive NMDA receptor blocker (memantine) to prevent this effect (1,2,3). The effects of orally administered MSG (250g/body weight) were investigated in adult female Wistar rats. The animals were divided into two groups (n=8 each) and served as their own controls. Animals were fed rat chow with either 0 or 2.5g MSG per day with or without memantine added (2mg/day), during alternate periods of 2 weeks. The sequence of food types was different in each group. Group 1 first received normal rat chow for 2 weeks (Control group), then chow with MSG (2.5g per day; MSG group) and finally chow with the same amount of MSG plus memantine (MSG-MEM group). Group 2 was submitted first to chow with MSG (MSG) for 2 weeks, then to chow with the same amount of MSG plus memantine (MSG-MEM) and finally to the standard food for 2 weeks (Control). Food intake of the animals was recorded in each period and blood samples of group 1 were taken from the jugular vein at the end of each diet period for hormonal levels determinations. All data were expressed as the mean ± SEM. To determine statistical differences, one-way ANOVA test for repeated measure was performed and differences among groups were subjected to contrast analysis test. Independently of the position in the sequence, during the periods of administration of MSG a significant increase in food consumption was seen: 8.1 ± 0.3 vs 5.6 ± 0.1 g/100 g BW; p= 0.006 and 9.7 ± 0.3 vs 8.1 ± 0.2 g/100 g BW; p=0.03 (MSG vs Control of Group 1 and Group 2, respectively). When MSG was given in the chow together with memantine, the food intake was significantly reduced reaching similar (Group 1) or lower (Group 2) levels than normal chow: 6.8 ± 0.7 vs 5,6 ± 0.1 g/100 g BW; p=0.06 (ns) and 6.7 ± 0.3 vs 8.1 ± 0.2 g/100 g BW; p=0.005 (MSG-MEM vs Control of Group 1 and Group 2, respectively). Similarly, significant increases in plasma adiponectin and CCK levels were observed in animals fed with MSG: 4.5 ± 0.3 vs 3.0 ± 0.2 µg/ml; p= 0.01 and 114.8 ± 3.5 vs 66.9 ± 10.0 pg/ml; p= 0.03 (MSG vs Control of Group 1 for adiponectin and CCK, respectively). Those effects were reversed also when memantine was added to the diet: 3.8 ± 0.3 vs 3.0 ± 0.2 µg/ml ; p= 0.1 (ns) for adiponectin and 58.18 ± 6.3 vs 66.84 ± 10.0 pg/ml; p=0.5 (ns) for CCK (MSG-MEM vs Control of Group 1). The effects observed in this experiment showed that MSG is able to increase voracity in adult animals, an effect reverted after the administration of memantine. These data actually confirm that by partially blocking the NMDA receptor, a reduction in voracity was obtained.