These studies investigated feeding responses to indirect activation of parabrachial cannabinoid CB1 receptors. Arachidonoyl serotonin (AA5HT), an inhibitor of the endocannabinoid degradative enzyme, fatty acid amide hydolase (FAAH), was infused into the parabrachial nucleus of Male Sprague-Dawley rats and intakes of high-fat/sucrose pellets and standard rodent chow were subsequently evaluated under various feeding schedules. FAAH blockade stimulated the intake of high-fat/sucrose pellets that were presented daily for 4hr during the light period, with compensatory decreases in the consumption of standard chow during the ensuing 20hr. These diet-selective changes repeated on the next day, indicating a shift in feeding towards the more palatable diet that lasted for 48hrs after a single infusion. The cannabinoid CB1 receptor antagonist, AM251, blocked the orexigenic actions of AA5HT, implicating CB1 receptors in mediating the feeding responses to FAAH inactivation. When the feeding schedule was reversed, AA5HT produced nominal increases in the consumption of standard chow for the 4hr access period, but substantial increases in the intake of high-fat/sucrose during the following 20hr interval. When presented with only high-fat/sucrose for 24hr, AA5HT increased 24hr food intake. In contrast, when given 24hr access only to standard chow, AA5HT failed to affect intake. Therefore, indirectly activating parabrachial CB1 receptors by blocking the degradation of native ligands selectively stimulates the intake of palatable food, with differential actions on total energy intake depending upon the feeding schedule. Our results support a role for parabrachial cannabinoid mechanisms in providing physiological regulation to neural substrates modulating feeding, energy balance and behavioral responses for natural reward.