The effects of intracerebroventricular (ICV) administration of neurotensin (NT) before a meal on intestinal postprandial motility were examined in conscious rats chronically fitted with intraparietal Nichrome electrodes in the duodeno-jejunum. The effects were compared with those of two analogues, [D-Tyr11]NT and [D-Trp11]NT, resistant to degradation by brain peptidases. NT (10 micrograms ICV) delayed the occurrence of postprandial disruption of duodenal motility and blocked it on the jejunum. [D-Tyr11]NT and [D-Trp11]NT (1 microgram ICV) elicited the same effects but at a ten-fold lower dose. NT administered peripherally just before a meal significantly lengthened the duration of the postprandial motor pattern. The central effect of NT on the fed pattern involved dopaminergic neurons as it was mimicked by dopamine, blocked by haloperidol and partly antagonized by either sulpiride or (+) SCH 23390. It is concluded that: 1) both D1 and D2 receptors are involved in the blocking effect of the postprandial disruption induced by central NT; 2) that [D-Tyr11]NT and [D-Trp11]NT are potent agonists at NT receptors in the brain.