International Journal of Comparative Psychology

We tested the ability of a beluga (Delphinapterus leucas) to imitate sounds presented to it. During the training session, we presented the subject three recorded sounds that were emitted by the subject, and the subject was trained to imitate them. The subject learned to correctly imitate the sounds. During the test session, two novel computer-generated artificial sounds were presented through an audio speaker. In addition, nine arbitrary vocal sounds produced by the experimenter were presented to the subject, and the subject was required to imitate them. Seven persons, who were not involved in the experiment, were presented the sample sounds and imitated calls; subsequently, they judged whether both sounds were similar to each other. In addition, sound spectrums of the sample sounds and imitated calls were analyzed. As a result, some components of the sound spectrums were similar, and most of imitated calls possess spectral features similar to the sample sounds. These results demonstrated that the beluga was able to correctly imitate novel sounds and spontaneously displayed aptitude for imitation.

During play fighting, rats attack and defend the nape, which if contacted is nuzzled with the snout. While all strains of rats can use all defensive tactics to protect the nape, there are strain-typical preferences for using particular tactics This study tests two hypotheses for this strain difference: (1) that each strain has strain-specific thresholds for each tactic, or (2) that each strain attacks differently which leads to strain differences in which defense tactics are used. Juvenile Long-Evans and Sprague-Dawley males were tested with both unfamiliar (experiment 1) and familiar (experiment 2) same-strain and different-strain partners. Experiment two was conducted to determine if familiarity with a different strain might allow rats to modify their strain-typical pattern of play. If hypothesis (1) were true, they would maintain strain-typical defense patterns irrespective of partner strain, whereas for (2) it would vary with partner strain. Hypothesis (1) was supported in the first experiment; all the rats maintained their strain-typical patterns regardless of the partner’s strain. However, the second experiment supported neither hypothesis, as each animal displayed strain-divergent behavior when playing with partners of a different strain as well as with partners of the same strain. Given that in the second experiment subjects were reared in mixed-strain groups, it is possible that, during the early juvenile period, animals are susceptible to discordant social experiences

The neurodegenerative disorder Huntington’s disease (HD) is characterized by motor dysfunction, cognitive impairment and psychiatric symptoms. The R6/2 (120 CAG repeats) mouse model of HD recapitulates many of the symptoms of the disease, including marked impairments in cognition and severe motor deficits. As cholinergic function has been reported to be affected in both HD patients and this mouse model, we tested whether treatment with the cholinesterase inhibitor donepezil could improve the R6/2 mice performance in the two-choice swim tank visual discrimination and reversal task. In this test mice are trained to swim towards a light cued platform located on one side of a water-filled tank. Once mice reach an acquisition criterion a reversal ensues. Wild-type and R6/2 mice were dosed with donepezil (0.6 mg/kg/day) or vehicle starting at 8 weeks of age and tested starting at 9 weeks of age. In experiment 1, vehicle-treated R6/2 mice showed a significant deficit during acquisition and reversal as compared to vehicle-treated WT mice. Donepezil improved reversal in the R6/2 group. In experiment 2, we confirmed the beneficial effect of donepezil on reversal in similar conditions. Donepezil had no effect on activity as measured in the open field test or through the latency to reach the platform during the swim test. We suggest that the donepezil-induced improvements in cognitive function observed in the R6/2 transgenic model of HD may reflect amelioration of deficits in cholinergic function that have been reported previously in this model. Further work is required to confirm the findings of these interesting although preliminary studies.

Reinforcement omission effects (ROEs) have beeninterpreted as behavioral transient facilitation after nonreinforcement inducedby primary frustration, and/or behavioral transient inhibition afterreinforcement induced by demotivation or temporal control. According to frustrationtheory, the size of the ROEs should depend directly on the reinforcementmagnitude: the behavioral facilitation after thereinforcement omission of larger magnitude should be greater than that observedafter the reinforcement omission of smaller magnitude. However, studiesinvolving operant paradigms have presenteddifficulty to demonstrate this relationship. Thus, the present study aimed toclarify the relationship between reinforcement magnitude and ROEsmanipulating the magnitude linked to discriminative stimuli in a partialreinforcement fixed interval schedule.  Rats were trained on a fixed-interval 12 s with limitedhold 6 s signaled schedule in which correct responses were always followed byone of two reinforcement magnitudes (0.5 and 0.05 ml of a 0.15% saccharinsolution). After acquisition of stable performance, the training was changedfrom 100% to 50% reinforcement schedules. The results showed that responserates were higher after omission than after reinforcement delivery. Besides,results showed that response rates were highest after the reinforcementomission of larger magnitude than of smaller magnitude. However, thefindings did not support the hypothesis that the reinforcement omission of largemagnitude induces greater behavioral facilitation than the reinforcementomission of smaller magnitude. The data were interpreted in terms of ROEsmultiple process behavioral facilitation after nonreinforcement and behavioraltransient inhibition after reinforcement.

This review focuses on reward-schedule effects, a family of learning phenomena involving surprising devaluations in reward quality or quantity (as in incentive contrast), and reward omissions (as in appetitive extinction), as studied in three taxonomic groups of vertebrates: mammals, birds, and amphibians. The largest database of dependable data comes from research with mammals in general, and with rats in particular. These experiments show a variety of behavioral adjustments to situations involving reward downshifts. For example, rats show disruption of instrumental and consummatory behavior directed at a small reward after receiving a substantially larger reward (called successive negative contrast, SNC)—a reward-schedule effect . However, instrumental SNC does not seem to occur when animals work for sucrose solutions—a reversed reward-schedule effect. Similar modes of adjustment have been reported in analogous experiments with avian and amphibian species. A review of the evidence suggests that carry-over signals across successive trials can acquire control over behavior under massed practice, but emotional memory is required to account for reward-schedule effects observed under widely spaced practice. There is evidence for an emotional component to reward-schedule effects in mammals, but similar evidence for other vertebrates is scanty and inconsistent. Progress in the comparative analysis of reward-schedule effects will require the intense study of a set of selected species, in selected reward-downshift situations, and aiming at identifying underlying neural mechanisms.

Reward loss experiences are among the main sources of emotional stress that humans face throughout their lives. In the animal laboratory, it has been repeatedly shown that the unexpected omission or devaluation of a reinforcer triggers a physiological, cognitive, and behavioral state called frustration. This state involves emotional mechanisms that resemble those unleashed by the presentation of other aversive stimuli, inducing similar stress responses through the activation of brain circuits involved in fear and anxiety. Although this hypothesis has been supported by behavioral, pharmacological, hormonal, and neurobiological evidence, only a few studies have focused on the neurogenetic basis of frustration in animals. This review focuses on the gene-environment interactions that determine the emotional response under conditions of reward loss. Behavioral and genetic correlates of frustration are reviewed in two strains of animals selected on the basis of extreme differences in active avoidance learning: inbred Roman High- (RHA-I) and Roman Low-Avoidance (RLA-I) rats. The review shows the usefulness of Roman strains for neurogenetic research and sets out unsolved questions regarding gene-environment interactions underlying behavior induced by incentive loss.

Human and animal studies have shown the long-lasting impact of early life experiences on the development of individual differences in stress responsiveness in later life. Despite the numerous works that evaluate the effect of early experiences on different behavioral paradigms, which for the most part are related to aversive situations, there are few studies that assess the effects on the unexpected downshift or omission of positive rewards. The purpose of this article is to present several independent lines of research into how frustration responses during adulthood may be influenced by early experiences. Very few works have been found on the subject, and in most cases the results were negative or controversial. However, more recent investigations suggest that the responses in adults to frustration or euphoria may be modulated by early experiences.

Frustration can be defined as an emotional state generated by the omission or devaluation in the quantity or quality of an expected appetitive reward. Thus reactivity to a reward is affected by prior experience with the different reinforcer values of that reward, a phenomenon known as incentive relativity, which can be studied by different paradigms to induce frustration. In this work we will focus in successive negative contrast (SNC), involving a downshift of the reward, and in the complete omission of the reward, a phenomenon known as extinction. Also, we will discuss the role of the neuroendocrine mechanisms involved in these processes. Specifically, we analyze the action of monoamines, adrenal and sexual hormones.

Rats emit aversive taste reactivity (TR) behavior (i.e., gapes) following intraoral delivery of a cocaine-paired taste cue, and greater conditioned aversive TR in well-trained rats predicts greater drug-taking. Here, we used a between-groups design and tracked the development of this conditioned aversive TR behavior on a trial by trial basis in an effort to determine when the change in behavior occurs and at what point individual differences in cue reactivity become predictive of cocaine-seeking and cocaine-taking. The results demonstrate that conditioned aversive TR to a cocaine-predictive flavor cue appears very early in training (i.e., following as few as 1 – 2 taste-drug pairings), stabilizes quickly, and becomes predictive of “terminal” self-administration within 3 – 4 trials. Indeed, rats exhibiting high conditioned aversive TR to the cocaine-paired cue also exhibited greater goal-directed behavior, were faster to take drug, self-administered more cocaine, and exhibited greater seeking during periods of drug non-availability. High conditioned aversive TR, then, develops quickly and is indicative of a greater motivation for drug.