Naloxone blocks that portion of feeding driven by sweet taste in food-restricted rats

We evaluated the potency of naloxone on intake of normal and sweet chow in food-deprived and schedule-fed rats. We found that naloxone's anorectic potency was dependent on the type of chow presented to the rats and the deprivation schedule utilized to stimulate food intake. In 24-h and 48-h deprived rats, naloxone decreased intake of normal rat chow at doses ranging from 0.3 to 3 mg/kg. In chronically deprived rats (80% of normal body wt), these doses of naloxone failed to decrease intake of normal chow. Rats eating sweet chow ate more when energy deprived and were more sensitive than rats eating normal chow to naloxone-induced limitations in food intake, both in acute and chronic food-deprived groups. Thus naloxone decreased intake of sweet chow much more effectively than normal chow even when rats were chronically food deprived. We also found that an extremely low dose of naloxone (0.03 mg/kg) decreased intake of sweet chow by almost 50% in satiated rats.

Persistent Behaviour in Extinction after Partial Deprivation in Training

Four groups of rats were trained to run an alleyway with one trial per day. Two groups were always deprived when trained while the other two received a partial deprivation schedule. One group of each pair received a continuous reward in the goal box while the other received partial reward. A partial reinforcement effect was found during extinction. The partially deprived groups also showed persistence in extinction. This result extends parallels between the effects of satiation and nonreward upon behaviour.

Adaptation to 23.5-Hr. Food and Water Deprivation Schedules in the Rat and Guinea Pig

20 rats and 20 guinea pigs were compared on a 23.5-hr. water-deprivation schedule and on a 23.5-hr. food-deprivation schedule. Rats showed a satisfactory adjustment to both these schedules, while guinea pigs adjusted to water-deprivation but not to the food-deprivation schedule.

Inhibition of ad Libitum Feeding in Rats by Salt Injections and Water Deprivation

Inhibition of ad libitum feeding in rats was induced by hypertonic NaCl injections. Though osmotic loads of sufficient size were capable of abolishing feeding completely for a time, the effect was not as large as had been predicted from a hypothesis of strictly linear subtractive inhibition. Feeding at a low level of hunger seems to be somewhat less affected by osmotic inhibition than feeding on a deprivation schedule. Inhibition of feeding was also produced by deprivation of water, and both the inhibition of food intake during deprivation, and the disinhibition by subsequent drinking indicated that the amount of inhibition of food intake is a non-linear (accelerating) function of water deficit. A model of the process indicating that the thirst signal undergoes a non-linear transformation before being subtracted from the signal corresponding to food demand is proposed.