Acquisition Of Schedule-induced Polydipsia Research Articles

The effects of apomorphine on the acquisition of schedule-induced polydipsia in rats

Injections of the dopamine agent, apomorphine, at the doses of 0.05 and 1.0 mg/kg were given to three different groups of rats while a fourth group received an injection of the drug vehicle. The injections preceded each of 15 schedule-induced polydipsia (SIP) acquisition sessions in which the subjects bar-pressed for food pellets on a fixed interval 60-sec schedule of reinforcement. The vehicle-injected group developed SIP over sessions while each dose of apomorphine suppressed the acquisition of SIP. Bar-press rates were also depressed at the higher doses, while response patterning was affected at the lower dose. The results support the contention that a normally functioning dopamine system is necessary for the acquisition of SIP, but they do not support the view that this neurotransmitter system is specifically involved in the generation of SIP.

Effects of naloxone, beta-endorphin and ACTH on acquisition of schedule-induced polydipsia.

A series of three experiments examined the possible involvement of endogenous opioid peptides in the development of schedule-induced polydipsia in rats. Repeated pretraining treatment with 2 mg/kg naloxone impaired acquisition of schedule-induced polydipsia, whereas the same treatment injected after training increased drinking. This later effect was time dependent, since a 30-min delay in the injection of naloxone resulted in a disappearance of its effect. Post-training injections of 10 micrograms/kg beta-endorphin or ACTH delayed the development of drinking. These findings are consistent with the hypothesis that endogenous opioid peptides modulate the development of schedule-induced polydipsia.

Effects of chronic d-amphetamine on the maintenance and acquisition of schedule-induced polydipsia in rats

The effects of chronic d-amphetamine on the acquisition of schedule-induced polydipsia and its maintenance by stimuli paired with food were evaluated in three interlocking experiments. In Experiment 1, polydipsia was induced in rats exposed to a response-independent fixed-time schedule in which a food pellet (US) was paired with a stimulus complex of lights and tone (CS) every 45 sec. When food was omitted and only the CS was presented rats drank very little water. Rats were then pretreated with 1 mg/kg d-amphetamine for 15 CS-US sessions and two or three subsequent CS-alone sessions. Animals remained polydipsic during CS-US sessions and drank little water during CS-alone sessions. However, d-amphetamine improved control exerted by the CS over drinking relative to no-drug sessions. In Experiment 2, acquisition of schedule-induced polydipsia during 10 sessions exposure to the periodic CS-US schedule was blocked in rats pretreated with 1 mg/kg d-amphetamine, compared with rats pretreated with buffer. During subsequent CS-alone sessions the temporal control of drinking by the CS was greater in the rats exposed to amphetamine. In Experiment 3, the rats that had not acquired polydipsia while under d-amphetamine in the previous experiment, all became polydipsic when pretreated with buffer. All rats remained polydipsic when re-exposed to amphetamine pretreatment. These results indicate that chronic d-amphetamine administration can facilitate control of licking and drinking by nonfood stimuli paired with food, and can block acquisition of schedule-induced polydipsia.

Schedule-induced polydipsia in F1 generation of wild/domestic Norway rats

The acquisition of schedule-induced polydipsia was examined in the F1 generation of a wild-caught male and a domestic female Norway rat in order to determine whether observed differences in drinking between feral and domestic strains involves a genetic component. Half of the crossbred litter drank like wild-caught rats and the remaining drank like domestic, laboratory reared rats. Implications for a genetic basis for schedule-induced polydipsia are noted and discussed.

Schedule-induced polydipsia in aged rats

The acquisition of schedule-induced polydipsia was examined in a group of 24-month old male rats. Five of the six rats did not develop polydipsia under a standard 80% body weight deprivation condition when tested on a fixed-time 1-min schedule of pellet delivery. As body weight was reduced from 80% to 70%, free-feeding weight, the remaining rats became polydipsic. These findings extend the generality of schedule-induced polydipsia to a population of aged rats, and also indicate that the motivational set point for generating adjunctive drinking changes as domestic rats age.

Delayed acquisition of schedule-induced polydipsia in rats with zona incerta lesions

Rats with lesions of the zona incerta (ZI) were hypodipsic under free-feeding conditions and were adipsic during periods of food deprivation. Lesioned rats did not differ from controls in daily food intake. In schedule-induced polydipsia (SIP) tests conducted by reducing the rats to 80% of free-feeding body weight and delivering 45 mg Noyes pellets on a fixed-time 1-min schedule, ZI lesions significantly delayed the acquisition of SIP. Both the size and frequency of post pellet drinking bouts were affected by the lesions. After 26 SIP sessions lesioned rats were drinking at levels similar to controls.

Acquisition of schedule-induced polydipsia in the mongolian gerbil

Three food-deprived Mongolian gerbils reliably displayed schedule-induced polydipsia when fixed-time food schedules were increased to 3-min interpellet intervals. No polydipsia was evident with shorter interpellet intervals. These data further extend the species generality of schedule-induced polydipsia, and indicate the importance of systematic variation of relevant variables before concluding that a given species does not display schedule-induced polydipsia.

Acquisition of schedule-induced polydipsia in rats with no prior drinking experience

Three litters of 10 rat pups each were reared on Purina laboratory chow and either (1) continuous access to water, (2) access to both water and lettuce until weaning at 21 days and then only lettuce, or (3) continous access to lettuce. At 100 days all rats were reduced to 80% free feeding weight and tested for polydipsia. During 15 sessions of polydipsia testing, excessive postpellet drinking developed in all groups to 45 mg Noyes pellets delivered on a fixed-time 1 min schedule. No significant differences in water intake over sessions were found among groups. It was concluded that schedule-induced polydipsia does not represent an exaggeration of a learned prandial drinking pattern, but rather an exaggeration of an inborn prandial drinking reflex.

The relationship of home cage feeding behavior to acquisition of schedule-induced polydipsia in the rat

Consummatory behavior was monitored in a group of naive rats in the home cage before and during testing on a fixed-time (FT) 60-sec schedule of reinforcement. Measures of the latency and frequency of drinking during a 30-min feeding session were recorded as well as home cage water consumption. The results revealed reliable correlations among pre-test measures of the latency to drink during feeding and home cage water intake with the rate of development of schedule-induced polydipsia (SIP). It was concluded that home cage feeding behavior is an important factor influencing the acquisition of SIP in the rat.

Licking response distributions associated with the acquisition of schedule-induced polydipsia

The relation between drinking and pellet delivery was examined in a rat that acquired polydipsia when it was exposed to a free fixed-interval (FFI) 50-sec food (Noyes 45-mg pellets) schedule. A distributional analysis of responding in the interpellet interval indicated that drinking, which was originally distributed equally throughout the interpellet interval, became concentrated predominantly as a postpellet event within the first FFI session. The redistribution of drinking as a postpellet event was followed by an increase in water consumption, with asymptotic water intake occurring by the fourth FFI session. These results indicated that schedule-induced polydipsia cannot be attributed to adventitious food reinforcement.

Effects of schedule, percent body weight, and magnitude of reinforcer on acquisition of schedule-induced polydipsia.

Two experiments with 43 Charles River (cd) male rats investigated the effects of schedule, percent body weight, and magnitude of reinforcer on the acquisition of schedule-induced polydipsia. A leaner reinforcement schedule induced greater polydipsia as did two non-schedule variables, reduced body weight and small magnitude of reinforcer. These findings, related to contemporary theories of schedule-induced polydipsia, emphasize the role of non-schedule variables in this behavior.