Abstract We previously reported that MK-801, a non-competitive N -methyl- d -aspartate (NMDA) receptor antagonist, increased food intake by rats. Increased intake occurred only when deprivation or presentation of a highly preferred food had initiated feeding. MK-801 did not cause initiation of food intake. We hypothesized that MK-801 might increase food intake by interfering with nutrient-related feedback signals generated during ingestion (within meal). To test this hypothesis, we administered MK-801 at several times during the course of a deprivation-induced meal. We found that MK-801, administered early in the meal, increased food intake dramatically, but only slightly when given late in a meal. The antagonist was ineffective for increasing intake when given after the meal had ended. In a second experiment, we examined the effect of MK-801 on deprivation-induced intake of 0·2% saccharin as compared to that of 15% sucrose, or sucrose adulterated with bitter sucrose octa acetate (SOA). MK-801 increased intake of 15% sucrose or sucrose adulterated with SOA. It did not increase intake of the sweet, non-nutritive 0·2% saccharin solution. These results suggest that NMDA receptors participate in the process of satiation and that MK-801 delays satiation by interfering with feedback from nutritive components of a meal.