Taste preconditioning augments odor-aversion learning.

On the basis of previous work that has shown a taste can potentiate odor-aversion conditioning in AX+ conditioning, 6 experiments used rats to examine the effects of pairing a preconditioned taste (A) with a novel odor cue (X) in an A+/AX+ aversion conditioning design. Experiments 1A and 1B demonstrated that a preconditioned taste produced a robust odor aversion that was significantly stronger than a potentiated odor aversion. The results of Experiment 2 showed that the robust odor aversion produced by A+/AX+ conditioning was not the result of the potentiated odor aversion summating with generalization from the taste aversion. The augmented odor aversion was produced only when the taste and odor stimuli were presented simultaneously (Experiment 3) and the preconditioned taste aversion was intact at compound conditioning (Experiment 4). Pairing a novel odor with a preconditioned taste was not sufficient to condition an aversion to odor (Experiment 5), although other results implicated a role for an association between odor and taste in the odor augmentation effect (Experiment 6). The present results have implications for current models of taste + odor interactions in flavor-aversion conditioning.

Augmentation, not blocking, in an A+/AX+ flavor-conditioning procedure.

An A+/AX+ Pavlovian conditioning design typically produces weakened or blocked conditioning to stimulus X. Two experiments were conducted in which rats first received an odor (A+) paired with an emetic US, and then received odor and taste (AX+) paired with the US. In both experiments, the preconditioned odor facilitated conditioning to the taste. In Experiment 1, a group that received two odor-illness pairings in A+ conditioning had a stronger taste aversion than a group that only had a single odor-illness pairing. Experiment 2 demonstrated that the strengthened taste aversion in the A+/AX+ condition was not due to stimulus generalization. The results represent a unique outcome in the flavor-aversion literature that is similar to potentiation. We propose that this facilitated conditioning to X in the A+/AX+ design be termed augmentation.

Augmentation of taste conditioning by a preconditioned odor.

Five experiments explored facilitated taste-aversion conditioning (odor-mediated taste augmentation), using rats that experienced odor (A) and taste (X) in an A+/AX+ design. Augmentation occurred when the stimuli were presented simultaneously during AX+ conditioning, and significantly weaker conditioning occurred after a sequential presentation (Experiment 1). Experiments 2 and 3 demonstrated that augmented conditioning decreased if the odor aversion was reduced through preexposure or extinction following A+ conditioning. A second-order conditioning explanation was not supported by the results of Experiment 4. Experiment 5 showed that extinction of the odor aversion after AX+ conditioning did not alter the strength of the augmented taste aversion. Odor-mediated taste augmentation is similar to potentiation, in which odor and taste cues operate in a synergistic, not competitive, manner.

Retention of context blocking in taste-aversion learning.

A series of experiments examined recovery from context blocking across a retention interval. In two flavor-aversion studies, rats received 0, 2, or 4 context + US pairings in Phase 1, a flavor + US pairing in Phase 2, and flavor testing after a 3-day or a 14-day retention interval. The procedures in Experimental 1 were performed in a novel context, whereas Experiment 2 was conducted in a moderately familiar context. In Experiment 1, the effects of 2 context + US pairing dissipated over the retention interval (i.e., the taste aversion increased in strength), but the effects of 4 context + US pairings did not change. In Experiment 2, no context blocking was observed after 2 context + US pairings, but the effects of 4 context + US pairings decreased across the retention interval. These studies are the first to show recovery from context blocking across a retention interval following single-element conditioning. Furthermore, Experiment 3 demonstrated that extinction of the context prior to taste conditioning eliminated context blocking, and Experiment 4 showed that weak taste aversions do not increase in strength across a retention interval. It is proposed that forgetting of the context-US association across an extended retention interval is the mechanism underlying recovery from context blocking.

Unconditioned stimulus intensity and retention interval effects.

In single-element taste-aversion learning, retention interval effects are seen if taste aversions are paradoxically weak when they are tested 1 day after conditioning than when they are tested 3 or more days after conditioning. One explanation of this phenomenon is that weaker taste aversions may increase in strength across a retention interval. To test this possibility, rats were given saccharin followed by an unconditioned stimulus (US) of weak, medium, or high intensity; testing occurred after a 1-day or a 5-day retention interval. The results showed retention-interval effects only at medium and high dosage levels, but not following a weak-intensity US. Furthermore, at the 5-day retention interval, aversion strength increased as the intensity of the US increased. However, at the 1-day retention interval, there were no significant differences due to US intensity. In accordance with previous experiments, this outcome suggests that nonassociative factors, such as US novelty, and not associative factors (e.g., US intensity), modulate taste aversion performance on a 1-day test.

Retention of rotationally induced taste aversions.

Retention interval effects are seen in single-element taste-aversion learning when taste aversions are significantly weaker if testing occurs 1 day after conditioning compared to tests conducted 3 or more days after conditioning. Since all previous demonstrations of this phenomenon have occurred following conditioning with the drug lithium chloride (LiCl), it was necessary to determine if the increased drinking at the 1-day interval was due to the aftereffects of LiCl. The present experiment explored the presence of retention interval differences following the use of a nonpharmacological unconditioned stimulus (US), rotational stimulation. Following a saccharin-rotation pairing, a saccharin aversion was seen at a 5-day testing interval, and this aversion was significantly stronger than the aversion observed at a 1-day test. Thus, these results are clear in showing that the retention interval effect occurs following conditioning with a nonpharmacological US, and this outcome allows for the refutation of an aftereffects of LiCl hypothesis.

Odor from rats tasting a signal of illness.

Rats running in a runway emit discriminable odors when encountering reward (R) or nonreward (N) goal events, and subsequent rats use these odors as discriminative stimuli to alter their approach speeds. In the present studies, a third goal event, aversively conditioned denatonium saccharide (A), was introduced. In Experiment 1, rats evidently emitted an odor when encountering the A goal event, because in the presence of this A odor subsequent conspecifics slowed their approach to the goal, much like their behavior on N trials. In Experiment 2, when N odor signaled R goal events and A odor signaled A goal events, rats approached quickly to N but slowly to A, indicating that they could discriminate N and A odors at the given concentrations. These studies indicate that rats emit an odor when confronted with a signal of impending illness and that this odor seems readily discriminable from R and N odors.

Triazolam attenuates amphetamine but not morphine conditioned place preferences.

In a series of four experiments the benzodiazepine triazolam was tested for reinforcing effects and for effects on reinforcement induced by amphetamine and morphine. Reinforcement was assessed in a conditioned place preference paradigm. Triazolam did not produce reinforcing or aversive effects when administered in doses ranging from 0.0625 to 0.5 mg/kg. Triazolam did attenuate reinforcing effects produced by 0.75 and 1.25 mg/kg amphetamine. No effect of triazolam was observed on morphine-induced reinforcement. These results indicate that the administration of triazolam can affect the brain mechanisms that mediate the reinforcing effects of amphetamine but not morphine.