Effects of preexposure flavor concentration on conditioned aversion and neophobia

In Experiment 1, 128 experimentally naive, water-deprived rats (Rattus norvegicus) received pretraining access to either 0.25 or 1.5% saccharin, distilled water, or 2.0% saline, followed either by a pairing of 0.25 or 1.5% saccharin with an intraperitoneal injection of 0.15 M lithium chloride (LiCl) or by a pairing of distilled water with LiCl. Preexposure to either saccharin concentration reliably reduced conditioned aversion effects to 0.25% saccharin, relative to that for preexposure to distilled water or saline. But only preexposure to 1.5% saccharin reduced aversion effects to that concentration. In Experiment 2, 48 naive, water-deprived rats received preexposure procedures as in Experiment 1. Afterwards, the rats were tested for neophobia to 0.25 or 1.5% saccharin. Neophobia was reliably greater to the 1.5% concentration. However, preexposure to either saccharin concentration obliterated evidence for neophobia to saccharin, relative to that following preexposure to distilled water or saline.     

Selective association learning in the rat: Generality of response system

Three experiments with rats examined the possibility that the cue-consequence specificity effect is not mediated by the conditioning of selective associations, but instead reflects the selective behavioral expression of taste-illness and exteroceptive-shock conditioning. Experiment 1 showed that the selective aversion performance could be obtained despite the use of locomotor withdrawal from the CS as the index of conditioning. Experiment 2 compared the response profiles of animals conditioned with footshock or illness to presentation of a saccharin or noise CS. During the test with the noise CS, lithium-conditioned subjects did not differ from control rats on any of several behavioral categories, but shock-conditioned rats showed high levels of freezing in response to the noise cue. During the saccharin test, lithium-treated rats engaged in behaviors such as chin wiping, head shaking, and gaping; these behaviors were rarely or never seen in shock-conditioned rats or controls, whose behavioral profiles during the saccharin test were almost identical. Experiment 3, using a blocking design, found that a noise-lithium pairing did not attenuate subsequent conditioning of a saline-lithium association, nor did a saccharin-shock pairing interfere with conditioning of a noise-shock association. These results confirm that the cue-consequence specificity effect is mediated by the selective associability of taste with illness and of exteroceptive cues with footshock.     

Conditioned and latent inhibition in taste-aversion learning: clarifying the role of learned safety.

Experiments 1-3 investigated the applicability of the classical conditioning concept of conditioned inhibition to taste-aversion learning. Rats made ill after drinking saccharin and subsequently administered a "safe" exposure to saline (or casein hydrolysate) evidenced an enhanced preference for the safe fluid (relative to either a third, slightly aversive, solution or to water) when compared to controls in which saccharin was not previously poisoned. Such active condition inhibition was significantly reduced in Experiment 4 when two safe exposures to saline preceded saccharin-illness pairings. These results indicate that conditioned inhibition can be established in a taste-aversion procedure and that a latent inhibition manipulation reduces the ability of a taste to become a signal for safety. Implications of these findings for the learned safety theory of taste-aversion learning and the relevance to bait-shyness of principles established within the classical conditioning paradigm are considered.     

Taste-mediated potentiation of noningestional stimuli in rats

Holtzman rats drank saccharin in a distinctive environmental chamber prior to lithium-induced toxicosis. This treatment was administered four times. These animals subsequently drank less water or familiar saline in the chamber than animals which received water in the environment during conditioning. In addition, these environmental stimuli blocked the formation of a lithium-mediated coffee aversion more if they were conditioned in the presence of saccharin than if they were conditioned in the presence of water. Such differential blocking provided further evidence that the presence of a taste during conditioning facilitated aversion learning to the environmental chamber.     

Effects of neophobia and habituation on the poison-induced avoidance of exteroceptive stimuli in the rat.

Two experiments on the role of neophobia in poison-induced aversions to exteroceptive stimuli are reported. In Experiment 1, rats were given either 10 or 25 days of habituation to the test situation prior to conditioning. Those animals with the longer habituation period avoided a complex of novel exteroceptive stimuli while those with the shorter habituation period did not. In Experiment 2 rats initially avoided the more novel of two containers, but gradually came to eat equal amounts from both. A single pairing of toxicosis with consumption from either the novel or the familiar container reinstated the avoidance of the novel container in both cases. The results were discussed in terms of an interaction between habituation and conditioning procedures. It was suggested that previously reported differences between interoceptive and exteroceptive conditioning effects may have been influenced by the differential novelty of the two classes of stimuli in the test situation. It was further suggested that non-contingently poisoned control groups should routinely be included in poison avoidance conditioning studies.     

Examination of factors which might disrupt a learned association between pentobarbital and LiCl

Injections of a sedative dose of pentobarbital (Pent) were followed 30 min later by injections of a toxic dose of lithium chloride (LiCl). As a result of these Pent →LiCl pairings, injections of Pent after consumption of saccharin solution failed to produce the usual saccharin aversion. This loss of the capacity of Pent to produce a flavor aversion is called Avfail. Experiment 1 showed that the Avfail effect was obtained with saccharin even though the rats consumed a novel vinegar solution prior to the Pent→LiCl pairings in Phase 1. This was surprising since the novel flavor was associated with the LiCl and ought to have overshadowed the association of Pent with LiCl. Experiment 2 showed that one set of Pent→LiCl pairings can produce two Avfail effects in sequence: the first with a novel flavor and the second with a flavor previously paired with LiCl sickness. It also showed that insertion of Pent injections and handling cues between the Pent→LiCl and the Flavor→Pent phases did not reduce the magnitude of Avfail. Experiment 3 showed that the Avfail effect was not disrupted by the insertion of 54 saline injections between the Pent→LiCl and Flavor→Pent pairings, nor by interposing 26 saline injections between each pair of Flavor→Pent trials. This seemed to exclude an important role for injection cues. Experiment 3 also showed that 4 exposures to Pent and 50 exposures to saline between the Pent→LiCl trials and the Flavor→Pent trials and 26 exposures to saline injections between each pair of Flavor→Pent trials did not reduce the magnitude of Avfail. The same exposure to Pent and saline injections did reduce the magnitude of the saccharin aversion shown by the LiCl→Pent group. These data are viewed as consistent with Lett's (Drug-drug associations: Evidence for the conditioning of a compensatory response. Paper presented at a meeting of the Eastern Psychological Association, New York, 1981) suggestion that Avfail represents a learned antisickness response.     

Potentiation and blocking of conditioned flavour and context aversions

Experiments 1, 2, and 3 demonstrated that the place in which rats had been made sick subsequently blocked the development of an aversion to a novel flavour that was presented in that place and paired with illness. These experiments also showed that a poisoned flavour subsequently potentiated the acquisition of an aversion to a novel place in which it was presented and paired with illness. Experiments 4 and 5 examined the hypothesis that the potentiation effect was mediated by the association between the place and the averted flavour rather than by the association between the place and the illness. However, there was no evidence that the place acquired aversive control over ingestive behaviours simply as a consequence of it having contained the averted flavour. Further, reinforcement of the aversive flavour outside the place-flavour compound increased flavour aversions but decreased, rather than increased, place aversions. These failures to detect evidence for an association between the place and the poisoned flavour led to a consideration of whether the animals were sensitive to the relation between the place and the poisoned flavour. Experiment 6 demonstrated that the potentiation effect was in fact contingent upon the relation between the place and the poisoned flavour, as was required by the view that the poisoned flavour had facilitated the association between the place and the illness.     

Potentiation and overshadowing in odor-aversion learning: Role of method of odor presentation,the distal-proximal cue distinction,and the conditionability of odor

Four experiments with rat subjects examined interactions between odors and tastes in compound aversion conditioning. In Experiments 1 and 2, a saccharin taste potentiated the conditioning of an almond odorant presented on a cup near the location of the drinking spout, but overshadowed the same odorant when it was mixed in drinking water. This difference depended on the type of odor administered during conditioning rather than testing (Experiment 2). Experiments 3 and 4 examined implications of two other differences between the cup and drink odors: (1) while the cup odor was a distal cue that suppressed approach to the spout, the drink odor was primarily a proximal cue that suppressed consumption, and (2) the cup odor was less conditionable than the drink odor when the stimuli were conditioned alone. In Experiment 3, unlike the proximal saccharin taste, the proximal drink odor failed to potentiate the conditioning of a different distal odor. In Experiment 4, substantial dilution of the proximal drink's concentration resulted in both weaker conditioning of the stimulus alone, and potentiation of its conditioning by saccharin. The results suggest that the difference in the conditionability of the cup and drink odors, and not their status as distal and proximal cues, may be critical in the production of potentiation. Weakly conditionable target stimuli are uniquely potentiated by saccharin.     

Drug states as discriminative stimuli in a flavor-aversion learning experiment

Injection of poison into rats after they drank in the presence of stimulus compounds of a drug state and a flavor resulted in little stimulus control by the drug state. In Experiment 1, half of the rats were poisoned after drinking salt water while stimulated with amphetamine and after drinking sugar water while sedated with pentobarbital, but they were not poisoned after salt-pentobarbital or sugar-amphetamine combinations. The other half were subjected to counterbalanced procedures. In abstract language, poisoning occurred after AX and BY stimulus combinations but did not occur after AY and BX combinations. In Experiment 2A, rats were poisoned only after consuming a particular flavored solution (salt or vinegar) in a particular state (pentobarbital or undrugged); that is, if AX was poisoned, BX, BY, and AY were experienced without poisoning. There was complete counterbalancing of flavors and drug states. Experiment 2B was similar except that amphetamine was used instead of pentobarbital. In both experiments, there was some discrimination learning based on the drug state, gut it was extremely weak.     

Odor as a conditioned inhibitor: Applicability of the Rescorla-Wagner model to feeding behavior

Hooded rats were given conditioned inhibition training in which the taste of saccharin alone was always followed by induced illness, but the taste of saccharin plus the odor of amyl acetate was not. In a series of three subsequent tests—summation, enhancement of conditioning, and retardation—it was demonstrated that the odor had acquired active inhibitory properties. The results paralleled those obtained with more traditionally studied stimuli and techniques and hence were found to be readily predictable from a recent model of conditioning set forth by Rescorla and Wagner (1972).     

Contextual control of fluid consumption: The effects of context extinction

Rats were trained on a conditional discrimination task in which saccharin was paired with LiCl in one context but paired with saline in another context. Rats drank less saccharin in the danger context than in the safe context, and consumption in the home cage was intermediate to consumption in the two training contexts. Rats also avoided the danger context on a choice test. After discrimination training, rats were given extinction trials with the danger context alone (Experiment 1 and 2) or with the danger context + water (Experiment 2). Extinction trials with the context + water abolished contextual control over saccharin consumption but not the avoidance of the danger context on the choice test. Extinction trials with the context alone abolished avoidance of the danger context but not contextual control over saccharin consumption. These data suggest that occasion setting, not simple context conditioning, is the mechanism by which contextual cues modulate fluid consumption.     

Characterization of a dose-response curve for nicotine-induced conditioned taste aversion in rats: relationship to elevation of plasma beta-endorphin concentration

In the first experiment a conditioned taste aversion paradigm was used to characterize a dose-response curve for the aversive properties of nicotine in male Sprague-Dawley rats. Doses of nicotine ranging from 0.01 to 0.46 mg/kg, 2.0 ml of 0.47 M lithium chloride, or saline were injected, ip, 10 min after exposure to a novel saccharin solution. Amount of saccharin consumed in a two-bottle test was assessed 72 h later. Nicotine doses of 0.046 mg/kg and above produced a significant degree of conditioned taste aversion. In a second experiment, four groups of 10 rats each were injected with saline, 0.022 mg/kg nicotine, 0.46 mg/kg nicotine, or 2.0 ml 0.47 of M LiCl. Doses of 0.46 mg/kg nicotine and 0.47 M LiCl elevated plasma beta-endorphin concentrations significantly above saline control values. The 0.022 mg/kg dose, the highest dose that did not produce conditioned taste aversion in Experiment 1, did not significantly increase plasma beta-endorphin concentrations. This finding suggests that doses of nicotine that produce conditioned taste aversion also promote the release of pituitary stress hormones. Taken together these data suggest that some of the pharmacological and behavioral effects attributed to nicotine, including the release of endogenous neuromodulators, may be dose-dependent concomitants of the aversive effects of nicotine in nicotine-naive animals.     

Determinants of the enhancement of flavored-water intake by prior exposure.

The intake of a 2.0% sodium saccharin solution in rats was observed to increase as a function of both the number (Experiment 1) and the duration (Experiment 3) of prior periods of access to the saccharin flavor, but did not increase when subjects were maintained on a fluid deprivation procedure in the absence of saccharin exposure (Experiment 2). The enhancement of intake was further influenced by the schedule of saccharin preexposures in the absence of variations in the amount of solution tasted (Experiment 4). The effect was not a function of the opportunity for subjects to determine their own pattern of contact with the saccharin flavor, the opportunity for association of the flavor with hunger and thirst reduction, or the amount of saccharin swallowed during preexposure (Experiment 5). These results suggest that mere exposure to a flavored solution is sufficient to increase subsequent intakes. The phenomenon is discussed in terms of the attenuation of neophobia elicited by the novelty of flavored solutions.     

Conditioned Inhibition Produced by Extinction of a Conditioned Stimulus

Four experiments used a conditioned taste aversion procedure to examine the potential for CS-alone extinction treatment to produce a conditioned stimulus that possesses inhibitory properties. In Experiment 1, saccharin was paired with LiCl, and then saccharin was presented alone for several trials to produce extensive behavioral extinction. Animals receiving this treatment were retarded in reacquiring conditioned responding to saccharin relative to control subjects receiving conditioning to the flavor for the first time. In Experiment 2, the extinguished saccharin stimulus was shown to decrease conditioned responding to a known excitor when the two stimuli were presented in compound as a summation test. Experiments 3A and 3B replicated the findings of Experiments 1 and 2 while providing evidence that the effects were not due to the differential effects of neophobia during testing. These three experiments revealed that an extinguished conditioned excitor passes retardation and summation tests for conditioned inhibition. Experiment 4 found that extinction of a known excitor was slowed when the excitor was extinguished in compound with a previously extinguished conditioned stimulus. That is, an extinguished CS provided protection from extinction to another CS, a finding also consistent with the view that extinction produces conditioned inhibition.     

Developmental flavor experience affects utilization of odor, not taste in toxiphobic conditioning

Feeding experiences were varied in developing rats and the effects upon flavor neophobia and lithium chloride-induced flavor aversions were observed. In Experiment 1, nursing experience of neonate rats was reduced by artificial feeding via intragastric cannula; the rats then were tested with apple juice paired with lithium chloride injection at weaning or maturity. Conditioned aversions were not affected, but neophobia to novel apple juice was attenuated in artificially-reared rats tested at maturity. In Experiment 2, rats received enriched feeding experience after weaning, which consisted of (a) obtaining many complex flavors, a few of which were paired with poisoning, effortlessly in the home cage, or (b) foraging for various foods on an elevated maze. No dramatic effects on neophobia or conditioned taste aversion for saccharin water were apparent. In Experiment 3, rats were given experience after weaning with vanilla-scented water either paired or unpaired with quinine water, and then tested with the odor of almond or that odor compounded with saccharin water for neophobia and lithium-induced aversions. Flavor-experienced rats exhibited more pronounced odor conditioning and more resistance to extinction of the odor aversion after both simple and compound conditioning. In contrast, saccharin taste aversions were relatively unchanged. Apparently, enriched feeding and drinking experience facilitates the utilization of odor more than taste cues.     

Effects of long- and variable-duration signals for food on activity,instrumental responding,and eating

Incentive-motivation theories typically assume that the conditioning of appetitive motivation involves the same parameters as Pavlovian salivary conditioning. In contrast, the Soltysik-Konorski model asserts that drive is inhibited by stimuli closely associated with food (salivary CSs) and augmented by stimuli more loosely associated with food (long and variable CS-US interval). Experiment 1 examined this latter proposition. Sixty-four rats were given extensive exposure to each of four environmental CSs, two while hungry and two while satiated. Within each deprivation condition, food was given 30–300 sec after placement of the rats in one environment, and was not given in the other environment. Performance on three separate measures—activity, lever-pressing, and food consumption—was higher in the environments previously associated with food. Experiment 2 examined the effects of discrete stimuli presented in advance of eating; in accord with the results of Experiment 1, food consumption was greater after a stimulus (1- to 9-min duration) previously paired with food than after no stimulus or after a stimulus unpaired with food. The overall results indicate (a) that stimuli associated with food become capable of facilitating a variety of food-directed behaviors, possibly via the conditioning of a common appetitive system, and (b) that a close association between the stimuli and food is not essential for such conditing to occur.     

Food choice in rats (Rattus norvegicus): the effect of exposure to a poisoned conspecific

Three experiments were conducted to examine the effects of exposure to a poisoned conspecific on subsequent food aversion in rats. In Experiment 1A, rats that had been aversively conditioned to a cocoa-flavored food were exposed to a poisoned conspecific that had eaten the same food. On the subsequent choice test, the animals increased their aversion to that food. These results were reconfirmed in Experiment 1B, in which a cinnamon-flavored food was used as the stimulus. In Experiment 2, subjects were first exposed to a poisoned conspecific and then conditioned to the food which the conspecific had eaten. On the test, they showed no sign of increased aversion to that food.     

Species-specific danger signals, endogenous opioid analgesia, and defensive behavior

The effects of handling stimuli and stress odors on species-specific defensive behavior and pain sensitivity were examined in rats. Animals not adapted to handling had longer jump latencies on the hot plate test of pain sensitivity than those with extensive handling experience. In a postshock freezing test, naltrexone enhanced defensive freezing relative to saline controls in nonadapted animals. However, naltrexone produced no such effect in rats that were adapted to handling. These two studies indicate that the handling procedure triggered an endogenous opioid analgesic response in rats not adapted to handling. Experiment 3 showed that a similar naltrexone-reversible opioid analgesia can be triggered by stress odors. Naltrexone, when compared to saline, enhanced postshock freezing in the presence of conspecific stress odors, but not in their absence. In Experiment 4, stress odors and nonadapted handling were able to activate defensive freezing directly, when tested in compound but not in isolation. The studies are consistent with the view that stress odors and handling stimuli are danger signals that activate endogenous opioid analgesia as well as defensive behavior, suggesting that analgesia is a component of the rat's defensive behavior system.     

Within-compound associations of taste and temperature

In two experiments, rats were given exposures to two solutions of different tastes (sucrose or sodium chloride) at two different temperatures (warm or cold). In Experiment 1, the rats were then given either one of the tastes at room temperature followed by LiCl injections, or distilled water at one of the temperatures followed by LiCl injections. Rats poisoned after drinking a taste were then given a choice between distilled water at the two temperatures, while those poisoned after drinking distilled water at a temperature were given a choice between the two flavors at room temperature. Rats drank less of the solution that contained the stimulus previously paired with the poisoned cue, demonstrating within-compound associations of tastes and temperatures. Experiment 2 found that tastes were better conditioned in a taste aversion procedure when the taste-temperature compound was the same during conditioning as during preexposure. This result is interpreted as evidence against a view of within-compound learning that treats the compound as a unitary stimulus.     

Signalling and incentive processes in instrumental reinforcer devaluation

We have previously reported that conditioning an aversion to the reinforcer using an isotonic lithium chloride (LiCl) solution following instrumental training reduces performance in a subsequent extinction test only if animals are re-exposed to the reinforcer prior to the test. Rescorla (1992), in contrast, reported an immediate devaluation effect using a hypertonic LiCl solution that did not depend upon re-exposure. In two experiments we examined the effect of using a hypertonic LiCl solution to condition the aversion to the reinforcer on subsequent instrumental performance in extinction, with and without re-exposure. In Experiment 1 thirsty rats were trained to press a lever for a sucrose solution before being injected with 0.6 M LiCl either immediately or after a delay. Half of the immediate and delay groups were then re-exposed to the sucrose in the absence of the lever, with the remainder being exposed to water. Contrary to the previously reported effects of isotonic LiCl, a hypertonic solution induced a reinforcer devaluation effect in all the immediately poisoned animals, which did not depend upon re-exposure to the reinforcer. In Experiment 2 the possibility that this devaluation effect was induced by the discomfort associated with the hypertonicity of the solution was assessed by replicating Experiment 1 but, in addition, using two immediately poisoned groups given the LiCl injection under anaesthesia. In the absence of anaesthesia, the devaluation effect observed without re-exposure to the reinforcer in Experiment 1 was replicated. When the injection was given under anaesthesia, however, a reinforcer devaluation effect was observed only in animals that were re-exposed to the reinforcer prior to the extinction test. These results were interpreted as evidence that a reinforcer devaluation effect induced by pairing the reinforcer with illness depends upon a process of incentive learning, whereas a devaluation effect mediated by learning a signalling relationship between the reinforcer and somatic discomfort does not.