Schedule-induced polydipsia in desalivate rats as a function of percent free-feeding weight

Physiology & Behavior, Vol. 24, pp. 65-71. Pergamon Press and Brain Research Publ., 1980. Printed in the U.S.A.

Schedule-Induced Polydipsia in Desalivate Rats As a Function of Percent Free-Feeding Weight TIMOTHY

R O E H R S A N D J O S E P H D. A L L E N

Psychology Department, University o f Georgia, Athens, GA 30602 R e c e i v e d 21 F e b r u a r y 1978 ROEHRS, T. AND J. D. ALLEN. Schedule-induced polydipsia in desalivate rats as a function of percent free-feeding weight. PHYSIOL. BEHAV. 24(1) 65--71, 1980.--Desalivate and control rats maintained at 80% of free-feeding weight were delivered 45 mg pellets on a fixed-time l-rain schedule for 14 sessions of polydipsia testing. Desalivate rats showed polydipsia immediately, but had lower asymptotic intakes than controls. Over the 14 polydipsia sessions postpellet bout size and frequency increased gradually in controls but remained stable in desalivates. Body weight increases to 105% of free-feeding weight over 21 additional sessions resulted in decreased intakes which were similar for desalivates and controls. In controls both bout size and frequency decreased as a function of body weight increases, while in desalivates only bout size decreased. The immediate acquisition of polydipsia in the desalivates was attributed to the prandial drinking pattern learned during postoperative recovery, whereas the attenuated levels of polydipsia were attributed to overhydration and consequent precise control of drinking bout size. Schedule-induced polydipsia

Prandiai drinking

Desalivate rats

S E V E R A L studies have investigated the role of orolingual factors in schedule-induced polydipsia (SIP) by disrupting normal sensory stimulation of the oral cavity through desalivation. Desalivate rats show immediate acquisition of SIP, but lower asymptotic levels of drinking than controls [9, I0]. By convention, if water intake during test sessions with intermittent delivery of food pellets is greater than intake when the same number of pellets is given all at once, the polydipsic drinking is considered schedule-induced [3]. Using such criteria, these previous studies of polydipsia acquisition in desalivates have demonstrated schedule induction since water intake during test sessions was at least three times that of baseline intake. The atypical response of the desalivate to polydipsia testing, however, raises a question as to whether the desalivate rat is showing SIP. Typically SIP is gradually acquired over the course of approximately two weeks of daily 30-min sessions [11]. In contrast the desalivate rat shows nearly asymptotic levels of water intake during the first session [9,10]. During the postoperative recovery following desalivation, desalivate rats acquire a prandial pattern of drinking in which a small draught of water is drunk immediately after a morsel of food is taken [7]. The immediate postpellet drinking of the desalivate rat during a polydipsia test would seem to be a result of the previously acquired prandial drinking pattern. Consequently the desalivate rat does not show the gradual acquisition of SIP which is characteristic of the intact rat. In fact desalivate rats not allowed to acquire a prandial drinking pattern showed a polydipsia acquisition rate similar to that of controls, but still showed attenuated polydipsia at asymptote

[10]. Thus one would expect the desalivate rat to have a smaller postpellet bout size and, if given recovery time to acquire a prandial drinking pattern, a greater probability of initiating postpeUet bouts than controls. Furthermore, if the polydipsia of the desalivate is due to a previously established drinking pattern, one might expect both bout size and frequency to remain constant over the normal polydipsia acquisition period. Available data are inconclusive as regards these questions [12]. Thus one purpose of the present study was to further analyze the response of the desalivate rat to a SIP test by examining the postpellet bout probability and size during the acquisition and maintenance of polydipsia. Another way to address the question as to whether the desalivate rat is showing SIP is to manipulate schedule variables critical to SIP. Two variables of principal importance to polydipsia are degree of intermittence in the delivery of food and food deprivation level. In the normal rat, session water intake is a bitonic function of fixed interval length [3]; however, in the desalivate rat, session intake has been found to be relatively insensitive to changes in interpellet interval [9]. This finding of insensitivity to variations in food intermittence further suggests that the polydipsia of the desalivate rat is due to factors other than schedule induction. Data for the desalivate rat on the other principal variable, food deprivation level, are not yet available. In the normal rat, the magnitude of SIP is a monotonically increasing function of food deprivation level [3]. Thus another purpose of the present study was to determine the effect of variations in the percentage of free-feeding body weight on the maintenance of SIP.

1portions of these data were presented at the annual meeting of the Psychonomic Society in Washington, D. C., November, 1977. Reprints should be addressed to Joseph D. Allen.

C o p y r i g h t © 1980 B r a i n R e s e a r c h P u b l i c a t i o n s Inc.--0031-9384/80/010065-07502.00/0

66

ROEHRS AND A L L E N

Desalivate rats show a general depression in response to several drinking challenges; the attenuated polydipsia in the desalivate rat has been attributed to this general depression [5]. It is argued that alterations in salivary composition affect the peripheral taste-receptor response and thus the intake of substances which normally stimulate these receptors. In support of this notion is the fact that desalivate rats have been reported to show depressed drinking during food deprivation and a variety of other dipsogenic stimuli [2, 4, 6, 8, 14], although no appreciable difference from controls in response to saline loads has been found [2, 6, 14]. A final purpose of the present study was to investigate the response of the desalivate rat to a variety of drinking challenges. METHOD

Animals Six male and six female, laboratory bred, Long Evans strain rats served as subjects. The animals were 105 to 110 days old at the start of the experiment. They were housed in individual cages with water continuously available and with a 12 hr light-dark cycle.

Apparatus Polydipsia testing and continuous 24 hr food and water intake recordings were conducted in Lehigh Valley Electronics (Model 1714) operant conditioning chambers with sound attenuated cubicles. In each chamber one LVE lever was mounted on the right corner of the front panel. Standard 45 mg Noyes pellets were delivered to a food magazine located in the center of the front panel. Water was available though a Richter drinking tube and 100 ml graduated cylinder located 4.0 cm to the right of the food magazine and 2.5 cm above the grid floor. The diameter of the aperture through which the tube protruded was 0.8 cm. Milliliters ingested during a session were recorded to the nearest 1.0 ml and licks at the tube were recorded with Grason-Stadler drinkometers (Model E 4690A). White noise was present during all sessions and a 6 W incandescent lamp illuminated the chamber. Chamber illumination during the continuous 24 hr recordings was synchronized with the 12 hr light-dark cycle of the home cage. Standard electro-mechanical programming and recording equipment was located in an adjacent room.

Procedure Surgery and home cage measures. Daily home cage food (ground Purina laboratory chow) and water intake was recorded for seven to ten days prior to surgery. All animals were anesthetized with Equithesin (0.25 cc/100 g, IP). Three males and three females, randomly chosen, were desalivated and the remaining animals served as controls. Desalivation was accomplished by ligation of the parotid ducts and extirpation of the submaxillary-sublingnal gland complex [10]. The ducts were ligated as they pass along the lateral surface of the masseter muscle and care was taken not to include the nearby ramus mandibularis nerve. The procedure for control animals involved an incision and exposure of the salivary glands. Following surgery daily food and water intake was measured for 14 days at which point all animals had regained their presurgery body weight levels. Polydipsia testing. For the polydipsia test, animals were reduced to 80% of their free-feeding body weights and maintained at that level for the first 17 days of testing. Baseline drinking was measured for three sessions by placing 30 pel-

lets in the food magazine at the beginning of a session and recording total session water intake (ml) and number of licks on the tube after 30 min. F o r the next 35 sessions 30 food pellets were delivered noncontingently at 1-min intervals. Total session water intake (ml), number of licks on the tube, number of bouts per session, and the temporal distribution of licking in the interpellet interval were recorded. Body weight was maintained at 80% for the first 14 sessions. Over the next 21 sessions, body weight was allowed to increase to 105% of free-feeding levels by gradually increasing the home cage portions. Home cage food portions were increased in a way that at least two polydipsia sessions each at 85, 90, 95, 100, and 105% of free-feeding body weight could be obtained. Drinking challenges. Following polydipsia testing, responses to a number of drinking challenges were measured. During this phase of the experiment animals had free access to food (Purina laboratory chow) and water except on test days. Animals were allowed to recover at least seven days after any test. The following tests were used: (1) total water intake (ml) during 24 hr food deprivation over three consecutive days, (2) 30 min water intake (ml) after 24 hr water deprivation, and (3) latency (sec) to the first drink upon access to 25 g food after 24 hr food deprivation. (4) Osmotic thirst: 1 ml/100 g of 2M saline was administered by intraperitoneal (IP) injection, food was removed and water intake recorded every 30 min for 6 hr. (5) Hypovolemic thirst: 5 ml of 30% polyethylene glycol (PG, 20,00 MW: Sigma Chemical Company) was administered by subcutaneous (SC) injection, food and water were withheld for 4 hr and then water was made available and intakes recorded every 30 rain for 2 hr. On alternate test days isotonic saline control injections were administered either IP or SC. Food was returned once the 30 min readings were completed and a final 24 hr intake was recorded. Ingestion patterns. Finally continuous 24 hr food and water intake recordings were obtained on two desalivate and two control animals. Approximately five days after being bar-press trained, animals were placed in the operant chamber for four to eight days with food (45 mg pellets delivered after a single bar press) and water available. Licks at the water tube and bar presses were recorded with an Esterline Angus event recorder and a Gerbrands cumulative recorder. The 24 hr sessions continued until daily intake values were similar to home cage values and two complete 24 hr records had been obtained. RESULTS

Home Cage Food and Water Intake The effect of desalivation on home cage food and water intake was assessed by separate two factor A N O V A s (mixed design) performed over the first nine postoperative days for each dependent variable. By the third day after desalivation mean dally food ration had stabilized at approximately 20 g, F(8,80)=10.34, p<0.001, above the presurgery and control levels. The increase in food ration was due to excessive spillage of food through the cage floor as had been reported previously for desalivate rats [7,13]. Mean daily water intake (ml) increased to more than twice that of baseline and control levels by the fifth postoperative day, F(8,80) = 6.60, p <0.001, and then dropped to a lower but elevated level. The increase in total daily water intake accompanied the acquisition of a prandial drinking pattern. Figure 1 illustrates the typical prandial drinking pattern of the desalivate rats as compared to the intake pattern of the controls obtained during the 24 hr

S-I-P IN D E S A L I V A T E S

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intake sessions. During these sessions the bout sizes averaged 0.12 ml for the two desalivates, which is comparable to the 0.10 ml per pellet reported previously for desalivates [7]. All desalivates had a latency to the first drink upon access to food following 24 hr food deprivation of 18 sec or less, while the shortest latency for control animals was 87 sec. The mean latency for desalivates was 11 sec and for controls it was 337 sec.

Polydipsia Acquisition Figure 2 presents mean session water intake for desalivates and controls during baseline and the first 14 days of polydipsia testing. With 30 pellets given all at once for a baseline measure of intake, controls drank a mean 2.24 ml and desalivates a mean 2.94 ml (approximately 0.1 ml per pellet) in 30 rain. With respect to baseline intake, both

groups developed excessive postpellet drinking during the polydipsia test, although the acquisition curves differed markedly. Desalivates drank four times the baseline level in the first polydipsia session~t=3.91, p<0.01, and intake was maintained at that level over the first 14 days of polydipsia testing. Mean session water intake for controls increased gradually reaching seven times baseline level by the sixth session, t=12.91, p<0.001. A two factor A N O V A (mixed design) performed over the first seven sessions revealed significant Sessions, F(6,61)=23.73, p<0.001, and Sessions by Groups effects, F(6,61)=15.40, p<0.001. An analysis of polydipsia acquisition in terms of the probability of postpellet drinking bouts (determined by recording the number of interpellet intervals containing licks) and postpellet bout size is presented in Fig. 3. After the first session desalivates drank after every pellet, consuming be-

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FIG. 4. Cumulative records of two desalivates and two controls for the first four polydipsia sessions ~tnd one session at the polydipsia asymptote. Pellet deliveries were recorded as oblique marks on the event marker and licks on the tube advanced the response pen which reset after each pellet delivery. tween 0.5 and 0.6 ml per pellet delivery (28 of the 29 recorded deliveries on session 2). Controls, on the other hand, drank 0.45 ml after each of less than half of the pellets delivered on the first session. By the sixth session controls were drinking after almost every pellet, consuming 0.8 ml per bout. The cumulative records in Fig. 4 depict the acquisition of schedule-induced drinking for two desalivate and two control rats during the first four polydipsia sessions and one of

the final three sessions where water intake had reached asymptote. The desalivates drank in the first session just as they drank at the polydipsia asymptote. Fully developed postpellet drinking bouts occurred after the first or second pellet delivery during the first session. Only one desalivate failed to drink consistently during the first session, which accounts for the depression in the first session's mean bout probability (see Fig. 3). In contrast, controls gradually in-

S-I-P IN DESALIVATES

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FIG. 7. Mean number of postpellet bouts (closed symbols) and mean ml per bout (open symbols) for desalivate (DS) and control (C) groups as a function of percent free-feeding body weight. creased bout frequency, bout size, and bout size uniformity with increased exposure to intermittent food delivery. When total session water intake had reached asymptote, over sessions 8 to 14, desalivates were drinking significantly less than controls, F(1,10) = 14.10, p <0.005. Postpellet drinking probability and bout size persisted at the values obtained for each group in session 6. The timing of a postpellet bout after a pellet delivery at the polydipsia asymptote is displayed in Fig. 5 as the distribution of licks within an interpellet interval. The mean percentage of licks which occurred in six consecutive 10-sec periods of the 1-min interpellet interval was calculated over sessions 10 to 14. The functions were very similar between groups and peaked at the second 10-sec segment of the interpellet interval. No statistically significant between group differences were found in an A N O V A performed on the mean number of licks occurring in each of six 10-sec periods. Desalivates and controls also did not differ significantly in lick efficiency, taking a mean of 0.0054 ( _+ 0.0015) and 0.0070 ( _+ 0.0022) ml per lick" respectively.

The effect of body weight gain on the maintenance of schedule-induced polydipsia is presented in Fig. 6. For both desalivates and controls, session water intake was a decreasing function of body weight increases to 105% of free-feeding weight, F(5,50)=41.0, p<0.001. The slope of the descending function was steeper for the control group than for the desalivate group, F(5,50)=6.15, p<0.001, and post hoc comparisons revealed specific between group differences at 80, 85 and 90% body weight. Figure 7 presents the mean ml per bout and the mean number of postpellet bouts as a function of percentage body weight gain. Desalivates continued to drink after almost every pellet delivery, but reduced the ml intake per bout from 0.5 to 0.25 ml as body weight increased to 105% of free-feeding levels. Controls decreased both bout frequency and bout size as body weight increased. At 105% of free-feeding weight controls had reduced bout size to a level slightly above that of desalivates, and drank after only 73% of pellet deliveries.

Drinking Challenges Table 1 presents the responses of desalivates and controls to various drinking challenges. There was a trend among desalivates to drink less than controls during the 30-min test following 24 hr water deprivation and during the three consecutive days of food deprivation. However, desalivate and control responses to cellular and extracellular thirst challenges were similar. Since the data did not meet the assumption of homogeneity of variance associated with the t distribution, group comparisons were made using the MannWhitney U test. The tests indicated that the median water intake (ml) in response to any of the drinking challenges did not differ significantly between groups. But, as might be expected, desalivates differed significantly from controls in mean latency (sec) to the first drink upon access to food following 24 hr food deprivation (11 and 337 sec respectively; U=0, p<0.001). DISCUSSION

In the present study, desalivate rats exhibited elevated postpellet drinking in the first session of intermittent pellet

70

ROEHRS A N D A L L E N TABLE 1

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delivery, but with continued sessions, intakes stabilized at a lower level than those of control rats. As such, these results directly replicated prior findings [9,10]. Both the probability and size of postpellet bouts remained essentially constant with desalivates, while both measures systematically increased with controls over the 14-session acquisition phase. In fact, desalivates engaged in a fully developed drinking bout following the first or second pellet delivery in the initial session. The fact that the drinking bout was virtually insensitive to continued exposure to a pellet delivery schedule suggests that the drinking displayed by desalivates is not schedule induced, except in the trivial sense. The added finding that session intakes with desalivates is relatively insensitive to changes in the interpellet interval [9] supports this position. However, water intake in the desalivates was markedly elevated when access to a constant number of food pellets was switched from continuous to intermittent. Assuming that the baseline sessions provided a control measure of intake produced by the desalivate's established pattern of prandial drinking, some parameters associated with the subsequently presented intermittent feeding schedule must have been responsible for the four fold increase in drinking. It was also found that session intakes with desalivates were sensitive to changes in food motivation, an interaction which is often used to infer the operation of schedule induction. The failure of the various standardly employed criteria to reach an agreeable decision in this study greatly complicates any interpretation of the findings. It questions not only the criterion measures which have been used to define schedule-induced polydipsia, but also the measures of the drinking behavior itself. For example, it would appear that the elevation in water intake following a claange from a free to an intermittent schedule of feeding is a sufficient criterion for defining the drinking as "polydipsic" but not as "schedule induced". Second, the development of a postpellet drinking pattern may also be a necessary but not sufficient indicant of schedule induction. Both desalivate and normal rats exhibited similar postpellet drinking patterns. Presumably, desalivates drank primarily to relieve symptoms of a dry mouth, where as the factors behind the postpellet drinking in

the intact rat remain obscure. Third, sensitivity to variations in food motivation is not necessarily an indication that polydipsia is schedule induced. F o o d motivation could be merely acting to energize any behavior which prevails in the situation. Measures which remain and would provide suitable criteria for inferring schedule induction would be (1) the gradual (i.e., session to session) changes in the drinking bout following transition from a free to a scheduled pellet delivery and (2) the continued sensitivity of the drinking bout to systematic changes in the pellet delivery schedule, such as the interpellet interval. Gradual increases in both the frequency and size of drinking bouts characterized the development of drinking over the first 14 sessions in intact rats, and it may be the concurrent increases in both of these bout parameters which is necessary to define schedule-induced drinking. The fact that bout frequency was constant in desalivate rats is due to a ceiling effect of having acquired a prandial drinking pattern in the home cage prior to polydipsia testing. When prandial drinking is initially prevented by testing desalivates immediately postsurgery [10], polydipsia is acquired at a rate similar to that of intact rats but still stabilizes at a lower intake. One might conclude, therefore, that a portion of the development of schedule-induced polydipsia lies in the acquisition of a prandial drinking pattern, that is, learning to initiate a drinking bout after each pellet delivery. The other portion lies in the gradual increase in bout size with continued exposure to the schedule, a phenomenon which was altogether lacking in desalivates. Bout sizes were initially similar in intact and desalivate rats (approximately 0.4 to 0.5 ml), but gradually doubled over 14 sessions for the intact rats while remaining virtually unchanged in desalivates. Desalivate and intact rats differed most importantly in regulating the size of the drinking bout. There are several factors which might be held responsible for constraining the bout size in the desalivate rat and which might therefore explain the failure to detect schedule-induced polydipsia in these animals. First, desalivates have been noted to lick at lower rates than intact rats [12], suggesting that their attenuated bout size could be due to difficulties with executing the lick response. In the present study, however, their lick efficiency, expressed in terms of volume ingested per lick, did not differ from that of intact rats, nor was their drinking distributed any differently within the interpellet interval. Thus licking inefficiency, when observed in desalivates, probably results from accidental damage to the ramus mandibularis nerve incurred during surgery. It has also been suggested that the attenuated intake of the desalivate rat during a SIP test is due to a general depression in response to any drinking challenge [5]. However, in the present study the drinking response of the desalivates was not reliably suppressed with any of the thirst challenges. According to the findings of Mendelson et al. [8] a marked but artifactual suppression in drinking should have been detected with both the food and water deprivation tests, since in both cases the desalivates alone should have entered the challenges with either an isoosmotic or hypoosmotic water balance. Indeed, there were trends toward the predicted suppression in just those two tests. Larger differences between the intakes of desalivates and controls were most probably over ridden by the carryover effect of the preceding polydipsia test experience. It has since been our experience that prior SIP testing regularly obliterates the effects of standard thirst challenges on lesioned preparations. A third and more plausible explanation is that, in con-

S-I-P IN DESALIVATES

71

junction with the acquisition of a prandial drinking pattern, the desalivate also learns to precisely meter and terminate a drinking bout. An oropharyngeal control of drinking in the classical sense of mouth metering recently has been given empirical support [1]. It has been demonstrated that the hydrational consequences of water intake can directly affect the oropharyngeal control of drinking. Sustained drinking of water in response to an 8-hr water deprivation challenge causes cellular overhydration within 15 min. When cellular overhydration occurs contiguous with drinking it serves as a potent inhibitor of further drinking. The desalivate rat, initially learning to drink water in order to facilitate the ingestion of dry food due to the lack of saliva, could be placing itself into extreme cellular overhydration within the time course of a meal. Thus the animal might learn to limit each drinking bout between bites of food to approximately 0.1 ml as opposed to the 0.5 to 2.5 ml bout consumed by a normal rat following a meal [4]. In the present study the daily water intake data of individual subjects supports this possibility. During postoperative recovery, mean daily water intake in each desalivate rat increased rapidly to a peak somewhere

above 100 ml for one or two days and then declined to a stable level twice that of control animals. The same rapid increase and subsequent decrease in daily water intake following desalivation has been reported by others [2,6]. Thus it is possible that the desalivate rat during postoperative recovery first learns to initiate a drinking bout following each bit of food, but then learns to terminate the bout after ingesting a small volume of water so as to minimize overhydration. Such precise bout size control may be carried over to the polydipsia session where the desalivate, unlike the normal rat, never increases, and possibly even decreases (see Fig. 4), its bout size with continued exposure to the food schedule. An adequate test of this proposition would require that desalivates be maintained on a wet mash or liquid diet following surgery and not allowed simultaneous access to dry food and water outside of the polydipsia session. Presumably such animals would never experience extreme cellular overhydration, never learn to precisely control bout size, and thus show an acquisition rate and asymptotic level of polydipsia similar to that of controls.

REFERENCES 1. Blass, E. M. and W. G. Hall. Drinking termination: Interactions among hydrational orogastric, and behavioral controls in rats. Psychol. Rev. 83: 356-374, 1976. 2. Epstein, A. N., D. Spector, A. Samman and C. Goldblum. Exaggerated prandial drinking in the rat without salivary glands. Nature 201: 1342-1343, 1964. 3. Falk, J. L. Conditions producing psychogenic polydipsia in animals. Ann. N. Y. Acad. Sci. 157: 369-593, 1969. 4. Falk, J. L. and R. W. Bryant. Salivarectomy: Effect on drinking produced by isoproterenol, diazoxide, and NaCl loads. Pharmac. Biochem. Behav. 1: 207-210, 1973. 5. Freed, W. J., F. R. Zec and J. Mendelson. Schedule-induced polydipsia: The role of orolinguai factors and a new hypothesis. In: Drinking Behavior, Oral Stimulation, Reinforcement, and Preference, edited by J. Weijnen and J. Mendelson. New York: Plenum Publishing Corporation, 1977. 6. Gutman, Y., P. Livneh and J. Pietrokovski. Role of salivary glands in response to thirst stimuli. Israel J. med. Sci. 6: 573575, 1970. 7. Kissileff, H. R. Oropharyngeal control of prandial drinking. J. comp. physiol. Psychol. 67: 309-319, 1969. 8. Mendelson, J., R. Zec and D. Chillag. Effects of desalivation on drinking and air licking induced by water deprivation and hypertonic saline injections. J. comp. physiol. Psychol. 80: 30-42, 1972.

9. Murphy, L. R. and T. S. Brown. Effects of desalivation on schedule-induced polydipsia. J. exp. Psyehol.: Anim. Behav. 1: 309-317, 1975. 10. Murphy, L. R. and T. S. Brown. Influence of prandial drinking vs dry mouth in the attenuation of SIP in the desalivate rat. Behav. Biol. 17: 529-545, 1976. 11. Roehrs, T. and J. D. Allen. The effects of zona incerta lesions on schedule-induced polydipsia. Paper read at the annual meeting of the Eastern Psychological Association, Boston, 1977. 12. Schaeffer, R. W. The response of desalivate rats to a timedependent food reinforcement schedule. Physiol. Behav. 18: 895--899, 1977. 13. Stricker, E. M. Influence of saliva on feeding behavior in the rat. J. comp. physiol. Psychol. 70:103-112, 1970. 14. Vance, W. B. Observations on the role of salivary secretions in the regulation of food and fluid intake in the white rat. Psyehol. Monogr. 79: 1-22, 1965. 15. Wong, R. and L. Kraintz. Desalivation and saline ingestion in rats. Behav. Biol. 19: 130-134, 1977. 16. Wong, R. and L. Kraintz. Interlick interval distribution of desalivated and control rats. Behav. Biol. 21: 141-145, 1977.