Consummatory Successive Negative Contrast Research Articles

Frustrative nonreward: Detailed c-Fos expression patterns in the amygdala after consummatory successive negative contrast

The amygdala has been implicated in frustrative nonreward induced by unexpected reward downshifts, using paradigms like consummatory successive negative contrast (cSNC). However, existing evidence comes from experiments involving the central and basolateral nuclei on a broad level. Moreover, whether the amygdala’s involvement in reward downshift requires a cSNC effect (i.e., greater suppression in downshifted animals than in unshifted controls) or just consummatory suppression without a cSNC effect, remains unclear. Three groups were exposed to (1) a large reward disparity leading to a cSNC effect (32-to-2% sucrose), (2) a small reward disparity involving consummatory suppression in the absence of a cSNC effect (8-to-2% sucrose), and (3) an unshifted control (2% sucrose). Brains obtained after the first reward downshift session were processed for c-Fos expression, a protein often used as a marker for neural activation. c-Fos-positive cells were counted in the anterior, medial, and posterior portions (A/P axis) of ten regions of the rat basolateral, central, and medial amygdala. c-Fos expression was higher in 32-to-2% sucrose downshift animals than in the other two groups in four regions: the anterior and the medial lateral basal amygdala, the medial capsular central amygdala, and the anterior anterio-ventral medial amygdala. None of the areas exhibited differential c-Fos expression between the 8-to-2% sucrose downshift and the unshifted conditions. Thus, amygdala activation requires exposure to a substantial reward disparity. This approach has identified, for the first time, specific amygdala areas relevant to understand the cSNC effect, suggesting follow-up experiments aimed at testing the function of these regions in reward downshift.

Transfer between tasks involving frustrative nonreward in rats: From consummatory to instrumental successive negative contrast

In tasks involving frustrative nonreward, animals learn to expect a large reward and eventually the reward is unexpectedly (i.e., without signals) downshifted to a small reward. Rats exposed to such tasks exhibit a transient rejection of the reward (in consummatory successive negative contrast, cSNC), or a transient deterioration of anticipatory behavior (in instrumental successive negative contrast, iSNC). When these tasks are administered in series, animals trained first in the cSNC task exhibit a reduced iSNC effect. This cSNC-to-iSNC transfer effect has been attributed to counterconditioning learning during cSNC postshift sessions, that is, to pairings of anticipatory frustration (a negative emotional response) with a reward. This hypothesis was tested in two experiments that manipulated the number of postshift trials in a cSNC task (Phase 1) before switching animals to the iSNC task (Phase 2). In these experiments, animals that received a single downshift session in the cSNC task (Phase 1) exhibited a stronger iSNC effect (Phase 2) than animals that had received either five (Experiment 1) or eight (Experiment 2) downshift sessions. More extensive downshift experience created more opportunities to develop counterconditioning. These results lend support to a role of counterconditioning in the recovery from reward downshift and in the development of transfer effects across reward downshift tasks that differ in terms of response requirements, reward type, and contextual cues.

Open field activity is linked to, but is not affected by, the rate of recovery from reward downshift in female Wistar rats

Frustration is an aversive emotion triggered by unexpected reward downshifts. Using the consummatory successive negative contrast (cSNC) task, a 32-to-2% sucrose downshift was shown to initially suppress consummatory behavior. Such suppression was followed by behavioral recovery over subsequent sessions. Individual differences often emerge in the rate of recovery after the initial consummatory suppression. These experiments were designed to determine whether a stable trait of sensation/novelty seeking (SNS) is related to such individual differences in recovery from reward downshift. In Experiment 1, open field (OF) activity in the central area served as a measure of SNS. A week later, animals received training in the cSNC task involving ten 5-min sessions of access to 32% sucrose followed by four sessions of access to 2% sucrose. Higher OF activity predicted greater consummatory suppression after downshift, but a steeper recovery rate across downshifted sessions. Controls not exposed to the OF showed cSNC, but downshifted animals performed at equivalent levels whether they had OF exposure or not. In Experiment 2, after a 32-to-2% sucrose downshift, fast vs. slow recovery animals displayed similar levels of central activity in the OF. In Experiment 3, animals exhibited similar levels of central activity whether after a 32-to-2% or an 8-to-2% sucrose downshift. In both experiments, activity levels were similar whether immediately after session 12 (onset of recovery) or after session 15 (fully recovered). These results suggest that individual variations in recovery from reward downshift are correlated with levels of SNS as a stable trait.

Ketamine retards recovery from reward downshift and supports conditioned taste aversion

Ketamine is a noncompetitive N-methyl-d-aspartate (NMDA) receptor antagonist with antidepressant, anxiolytic, and memory effects in clinical and preclinical studies. The present studies investigated the behavioral effects of ketamine in animals exposed to a consummatory successive negative contrast (cSNC) task involving unexpected reward downshift, negative emotion (frustration), and aversive memory. Food-restricted male rats had 5-min access to 32 % sucrose in each of 10 preshift sessions followed by 4 % sucrose in 4 postshift sessions. Unshifted controls had access to 4 % sucrose during all 14 sessions. Ketamine (10 mg/kg, ip) was injected 30 min before sessions 11 and 12 (Experiment 1) or immediately after session 11 (Experiment 3). The results showed that both pre- and postdownshift session injection of ketamine increased consummatory suppression, as Group 32-4/Ket exhibited lower sucrose intake than Groups 32-4/Sal, 4-4/Ket, and 4-4/Sal. These effects extended beyond the day(s) of injection. Experiments 2 and 4 showed that the same dose, route of administration, and time of injection induced significant conditioned taste aversion to 4 % sucrose, in the absence of reward downshift. These data suggest that ketamine induces an aversive state that may summate with frustration induced by reward downshift in the cSNC task and also support a conditioned taste aversion to 4 % sucrose in the absence of reward downshift. Implications for these and other experiments involving pre- and postsession administration of ketamine are discussed.

When loss hurts: Psychobiological basis of frustration

Frustration or psychological pain refers to a negative emotional experience derived from unexpected incentive loss. The scientific study of frustration with non-human animals is abundant and consistent, whereas human research on this topic seems to be more fragmentary because of the variety of conceptual, theoretical and experimental approaches. The main aim of this paper was to conduct a narrative review of the scientific literature about the psychological construct of frustration. With this goal in mind, we first described the consummatory successive negative contrast, a widely used animal model of psychological pain and frustration. We also conducted a systematic search of experimental studies aimed at inducing frustration in humans, reviewed studies focused on analyzing the relationship between physical and psychological pain, and selected experiments involving the manipulation (omission, devaluation) of social stimuli. A discussion of the implications of the results for basic and clinical research was finally included, with an especial emphasis in the current COVID-19 pandemic, a worldwide experience of incentive loss with relevant psychological consequences.

High Alcohol-Preferring Mice Show Reaction to Loss of Ethanol Reward Following Repeated Binge Drinking.

Beyond yielding high blood ethanol (EtOH) concentrations (BECs), binge-drinking models allow examination of drinking patterns which may be associated with EtOH's rewarding effects, including front-loading and consummatory successive negative contrast (cSNC), a decrease in intake when only water is available to subjects expecting EtOH. The goals of the current study were to broaden our understanding of these reward-related behaviors during binge EtOH access in high alcohol-preferring (HAP) replicate lines (HAP2 and HAP3) of mice selectively bred to prefer alcohol. We hypothesized that both lines would show evidence of front-loading during binge EtOH access and that we would find a cSNC effect in groups where EtOH was replaced with water, as these results have been shown previously in HAP1 mice. HAP replicate 2 and replicate 3 female and male mice were given 2hours of EtOH or water access in the home cage for 15 consecutive days using "drinking in the dark" (DID) procedures. Mice received the same fluid (either 20% unsweetened EtOH or water) for the first 14days. However, on the 15th day, half of the mice from these 2 groups were provided with the opposite assigned fluid (EtOH groups received water and vice versa). Intake was measured in 1-minute bins using specialized sipper tubes, which allowed within-session analyses of binge-drinking patterns. EtOH front-loading was observed in both replicates. HAP3 mice displayed front-loading on the first day of EtOH access, whereas front-loading developed following alcohol experience in HAP2 mice, which may suggest differences in initial sensitivity to EtOH reward. Consummatory SNC, which manifests as lower water intake in mice expecting EtOH as compared to mice expecting water, was observed in both replicates. These findings increase confidence that defined changes in home cage consummatory behavior are driven by the incentive value of EtOH. The presence of cSNC across HAP replicates indicates that this reaction to loss of reward is genetically mediated, which suggests that there is a biological mechanism that might be targeted.

Dimensions of sucrose solutions in the successive negative contrast effect

The consummatory successive negative contrast (cSNC) task typically involves administering food-deprived rats 10 daily 5-min sessions of access to 32 % sucrose (preshift) followed by a few sessions in which the concentration is reduced to 4 % sucrose (postshift). Such sucrose downshift leads to transient suppression of consummatory behavior. Reward downshifts were used to determine whether food-deprived rats treat sucrose solutions as food, because sweetness is a proxy for its caloric content, or as water, because a solution has hydration content. In Experiment 1, a cSNC effect was obtained in food-deprived animals, but not in water-deprived animals. This suggested that food deprivation focused attention on the feeding dimension of sucrose, whereas water deprivation focused attention on the drinking dimension of sucrose. Sucrose downshift results in a greater caloric change than in hydration content because both concentrations continue to provide fluid. Experiments 2 and 3 offered presession access to rewards either before preshift or before postshift sessions, respectively. Consistent with this attentional view, presession access to water (which should focus attention on the feeding dimension), but not to food (which should focus attention on the drinking dimension), suppressed consummatory behavior after a sucrose downshift. Presession access to food, like water deprivation, enhanced the hydration properties of the sucrose solution at the expense of its caloric properties. These results are consistent with an attentional hypothesis according to which the internal state, manipulated via deprivation or presession reward access, determines which dimension of the sucrose reward would control consummatory behavior.

Frustrative nonreward: Chemogenetic inactivation of the central amygdala abolishes the effect of reward downshift without affecting alcohol intake.

The role of the central amygdala (CeA) in the adjustment to a 32-to-2% sucrose downshift in the consummatory successive negative contrast (cSNC) task and in a free-choice 10% alcohol-water preference task (PT) was studied using chemogenetic inactivation. cSNC is a model of frustrative nonreward that enhances alcohol consumption. In Experiment 1, sessions 1-10 involved 5-min access to 32% sucrose and sessions 11-12 involved access to 2% sucrose. Vehicle or clozapine N-oxide (CNO; 1 or 3mg/kg, ip), used later to activate the inhibitory designer receptor, was administered 30min before sessions 11-12. There was no evidence that CNO affected consummatory behavior after the sucrose downshift. In Experiment 2, all animals received an infusion of the inhibitory designer receptor hM4D(Gi) into the CeA. After recovery, animals received access to either 32% or 2% sucrose on sessions 1-10, followed by 2% sucrose on sessions 11-12. Immediately after each 5-min sucrose session, animals received a 2-bottle, 1-h PT with 10% alcohol and water. CNO (3mg/kg, ip) or vehicle was administered 30min before sessions 11-12. CeA inactivation prior to sucrose downshift eliminated the cSNC effect, which was observed in vehicle controls. However, there was no evidence that CeA inactivation affected preference for 10% alcohol over water. These results support the hypothesis that CeA activity is critical for cSNC effect, an outcome consistent with the view that the amygdala plays a central role in frustrative nonreward.

Emotional Reactivity to Incentive Downshift in Adult Rats Exposed to Binge-Like Ethanol Exposure During Adolescence.

Alcohol use in adolescents is often characterized by binge-like ethanol consumption pattern, which is associated with long-term health consequences and even with important harms to his developing brain. Among this, ethanol exposure induces long-lasting alterations in anxiety-related neurobiological systems such as corticotropin releasing factor (CRF) or melanocortin system (MC). Recently, it has been demonstrated that adult rats exposed to adolescent intermittent ethanol (AIE) exposure exhibited anxiogenic-like behavior. Given that it has been demonstrated that negative affective state is relevant to development of addictive behavior, it is tempting to suggest that increased risk of adult abusive alcohol use exhibited in rats exposed to ethanol during adolescence may be related with differences in anxiety-related behavior. We conducted a study investigating the emotional reactivity after a reward devaluation (12-to-1 pellet or 32-to-4% sucrose downshift) in adult rats exposed to binge-like ethanol exposure during adolescence. For this aim, adolescent Sprague-Dawley rats were treated with ethanol (2.5 g/kg ip; AIE) or saline (AIS) for 2 consecutive days at 48-h intervals over a 14-day period (PND30-PND43). Following 25 free-ethanol days, adult rats were trained in consummatory and instrumental successive negative contrast task (cSNC and iSNC). Our data shows that both AIE and AIS groups exhibited suppression of the consummatory and instrumental behavior after reward devaluation relative to unshifthed control. Also, adult rats exposed to alcohol during adolescence exhibited a particularly strong negative affective state (lower sucrose consumption) with regards to the AIS group in the cSNC. This data demonstrated that adolescent binge-like ethanol exposure might trigger a greater emotional reactivity following incentive downshift, which might be linked to higher vulnerability to substance use disorder.

Assessing the External Validity of Successive Negative Contrast – Implications for Animal Welfare

ABSTRACTWhen unexpectedly switched from a preferred to a less-preferred food reward, non-human animals may decrease consumption below that when only receiving the less-preferred reward – a successive negative contrast (SNC) effect. SNC has been proposed as an animal welfare indicator, however, to be effective it should show external validity; being demonstrable outside of highly standardized laboratory settings. We therefore investigated whether the SNC effect typically shown in laboratory rats was observed in owned (pet) rats from heterogeneous non-laboratory environments. Subjects (N = 14) were tested in a consummatory SNC paradigm with solid food rewards. “Shifted” rats received a high-value reward for 10 days (pre-shift), a low-value reward for six days (post-shift), then one additional day of high-value reward (re-shift). “Unshifted” rats always received the same low-value reward. “Shifted” rats consumed more food during pre-shift and re-shift trials, but ate less of the low-value food than “unshifted” animals in the post-shift trials – a SNC effect. This confirms the external validity of the SNC paradigm, extending reproducibility to outside the laboratory, indicating translatability across contexts, thus enhancing its potential use as a welfare indicator.

Consummatory Successive Negative Contrast in Rats.

Using animal models in addiction and pain research is pivotal to unravel new pathways and mechanisms for the treatment of these disorders. Reward devaluation through a consummatory successive negative contrast (cSNC) task has shown the ability to reduce physical pain sensitivity (hypoalgesia) and increase oral ethanol consumption in rats. The procedure is based on exposing the experimental animals to a 32% sucrose solution during several sessions (preshift sessions) followed by a devaluation to 4% sucrose during the next few sessions (postshift sessions). The cSNC effect can be monitored by comparing the experimental group to an unshifted control that had access to 4% sucrose throughout the entire experiment (preshift and postshift sessions). The cSNC phenomenon is defined by lower consumption of sucrose in the downshifted group than in the unshifted group during postshfit sessions.

Correlación entre Miedo Incondicionado y la Primera Reacción a la Disminución y Extinción de un Reforzador Apetitivo

Cuando las ratas tienen acceso a una solución azucarada al 32% y luego la concentración disminuye al 4%, los animales consumen o permanecen en contacto con el bebedero menos tiempo que los animales que siempre consumieron la solución al 4%. A este fenómeno de Contraste Sucesivo Negativo consumatorio (CSNc) se le considera un modelo animal de frustración. Existe evidencia de que en una prueba de luz-oscuridad, las ratas prefieren permanecer en el compartimiento oscuro, lo que sugiere una respuesta de miedo incondicionado hacia lugares claros. Se presentan dos experimentos en los que se evaluó la preferencia de ratas en una prueba de luz-oscuridad y a un CSNc (Experimento 1) y a una Extinción Consumatoria (Ec, acceso a un bebedero vacío, Experimento 2) para evaluar la correlación entre la primera reacción a la devaluación u omisión de reforzadores con las respuestas de miedo incondicionado a los lugares oscuros. Las ratas que permanecieron más tiempo en el lugar oscuro permanecieron menos tiempo en contacto con el bebedero durante el primer ensayo de devaluación del reforzador (Experimento 1) y durante el primer minuto del primer ensayo de Ec (Experimento 2). Esos resultados se discuten en relación con las teorías de Amsel (1958), Gray (1987) y Flaherty (1996).

Two profiles in the recovery of reward devaluation in rats: Latent class growth analysis

Consummatory successive negative contrast (cSNC) occurs when animals exposed to an unexpected downshift from a high palatable reward (e.g., 32% sucrose solution) to a less preferred one (e.g., 4% sucrose solution) show an abrupt and transient suppression of the consummatory response, compared with control animals that always had access to the less preferred one. This phenomenon constitutes an animal model of stress produced by frustrative events. To obtain information about individual differences regarding cSNC, we used Latent Class Growth Analysis (LCGA) to analyze a sample of 53 animals exposed to an incentive downshift. We found two profiles of animals, both showing the suppression of the consummatory response but diverging in the speed of the recovery. Our results are consistent with previous literature showing individual differences in cSNC and do not support the existence of a third profile.

Transfer between anticipatory and consummatory tasks involving reward loss

Does recovery from reward devaluation or partial reinforcement (PR) involve the counterconditioning of frustration? Transfer among tasks involving reward loss was used to uncover frustration counterconditioning. In Experiment 1, Phase 1 training in consummatory successive negative contrast (cSNC; 32-to-4% sucrose devaluation) eliminated Phase 2 iSNC in one-way avoidance (40-to-3 s safety-time reduction), but the opposite sequence generated no detectable transfer. In Experiment 2, transfer from Phase 1 cSNC to Phase 2 autoshaping extinction after continuous reinforcement increased lever pressing in previously downshifted animals relative to unshifted controls. However, Phase 1 training in autoshaping under partial reinforcement (PR) had no effect on Phase 2 cSNC. Transfer from PR to cSNC also failed when sucrose pellets were used in autoshaping (Experiment 3), when autoshaping acquisition was extended from 100 to 300 trials (Experiment 4), and when preshift training in cSNC was extended from 10 to 20 sessions (Experiment 5). In Experiment 6, Phase 1 training in PR for licking enhanced Phased 2 cSNC, also involving licking, and in Experiment 7 Phase 1 PR training in autoshaping enhanced Phase 2 cSNC after a 22-to-4% sucrose downshift. Whereas prior exposure to cSNC (consummatory task) increased resistance to extinction in autoshaped lever pressing, prior training in one-way avoidance, PR in autoshaping, or PR in taste conditioning (all anticipatory tasks) either had no effect or they enhanced the cSNC effect. Frustration counterconditioning developed during these tasks, but the type of transfer effect depends on task sequence.

Consummatory successive negative contrast in rats: Assessment through orofacial taste reactivity responses

Rats exposed to a downshift from a large reward (32% sucrose) to a small reward (4% sucrose) show an abrupt and transient reduction in consumption in comparison with animals that are always exposed to the small reward. This effect is called consummatory Successive Negative Contrast (cSNC) and involves negative affective consequences that lead to an aversive emotional, cognitive and behavioral state of frustration. There are few previous works that have investigated the hedonic alterations that undergo an unexpected incentive devaluation. The hedonic impact of fluids can be reliably assessed by examining the orofacial reactions of acceptance and rejection in the taste reactivity (TR) test. This study addressed in male adult Wistar rats the hedonic impact of incentive devaluation in an adapted cSNC protocol. Specifically, the orofacial responses to a sucrose solution infused into the oral cavity were measured. It was observed that animals exposed to reward devaluation, from a 32% to a 4% sucrose solution, showed a decrease in the duration of appetitive responses (tongue protrusions, mouth movements, paw licks) as compared with subjects which only experienced the low concentration of sucrose. The results are consistent with the hypothesis that incentive devaluation in a cSNC not only results in reduced intake, but also in a reduction in the hedonic value or palatability of the devalued reward.

Reward loss and the basolateral amygdala: A function in reward comparisons

The neural circuitry underlying behavior in reward loss situations is poorly understood. We considered two such situations: reward devaluation (from large to small rewards) and reward omission (from large rewards to no rewards). There is evidence that the central nucleus of the amygdala (CeA) plays a role in the negative emotion accompanying reward loss. However, little is known about the function of the basolateral nucleus (BLA) in reward loss. Two hypotheses of BLA function in reward loss, negative emotion and reward comparisons, were tested in an experiment involving pretraining excitotoxic BLA lesions followed by training in four tasks: consummatory successive negative contrast (cSNC), autoshaping (AS) acquisition and extinction, anticipatory negative contrast (ANC), and open field testing (OF). Cell counts in the BLA (but not in the CeA) were significantly lower in animals with lesions vs. shams. BLA lesions eliminated cSNC and ANC, and accelerated extinction of lever pressing in AS. BLA lesions had no effect on OF testing: higher activity in the periphery than in the central area. This pattern of results provides support for the hypothesis that BLA neurons are important for reward comparison. The three affected tasks (cSNC, ANC, and AS extinction) involve reward comparisons. However, ANC does not seem to involve negative emotions and it was affected, whereas OF activity is known to involve negative emotion, but it was not affected. It is hypothesized that a circuit involving the thalamus, insular cortex, and BLA is critically involved in the mechanism comparing current and expected rewards.

Hypoalgesia Induced by Reward Devaluation in Rats

Reduced sensitivity to physical pain (hypoalgesia) has been reported after events involving reward devaluation. Reward devaluation was implemented in a consummatory successive negative contrast (cSNC) task. Food-deprived Wistar rats had access to 32% sucrose during 16 sessions followed by access to 4% sucrose during 3 additional sessions. An unshifted control group had access to 4% sucrose throughout the 19 sessions. Pain sensitivity was measured using von Frey filaments (Experiment 1) and Hargreaves thermal stimuli (Experiment 2) in pretraining baseline, 5 min, and 300 min after either the first (session 17) or second (session 18) devaluation session in the cSNC situation. Sucrose consumption was lower in downshifted groups relative to unshifted groups during postshift sessions—the cSNC effect. Hypoalgesia was observed in downshifted groups relative to unshifted controls when pain sensitivity was assessed 5 min after either the first or second devaluation session, regardless of the pain sensitivity test used. Both pain sensitivity tests yielded evidence of hypoalgesia 300 min after the second downshift session, but not 300 min after the first devaluation session. Whereas hypoalgesia was previously shown only after the second devaluation session, here we report evidence of hypoalgesia after both the first and second devaluation sessions using mechanical and thermal nociceptive stimuli. Moreover, the hypoalgesia observed 300 min after the second devaluation session in both experiments provides unique evidence of the effects of reward loss on sensitivity to physical pain 5 hours after the loss episode. The underlying neurobehavioral mechanisms remain to be identified.

Dorsomedial striatum lesions affect adjustment to reward uncertainty, but not to reward devaluation or omission

The dorsomedial striatum (DMS) has been implicated in the acquisition of reward representations, a proposal leading to the hypothesis that it should play a role in situations involving reward loss. We report the results of an experiment in which the effects of DMS excitotoxic lesions were tested in consummatory successive negative contrast (reward devaluation), autoshaping training with partial vs. continuous reinforcement (reward uncertainty), and appetitive extinction (reward omission). Animals with DMS lesions exhibited reduced lever pressing responding, but enhanced goal entries, during partial reinforcement training in autoshaping. However, they showed normal negative contrast, acquisition under continuous reinforcement (CR), appetitive extinction, and response facilitation in early extinction trials. Open-field testing also indicated normal motor behavior. Thus, DMS lesions selectively affected the behavioral adjustment to a situation involving reward uncertainty, producing a behavioral reorganization according to which goal tracking (goal entries) became predominant at the expense of sign tracking (lever pressing). This pattern of results shows that the function of the DMS in situations involving reward loss is not general, but restricted to reward uncertainty. We suggest that a nonassociative, drive-related process induced by reward uncertainty requires normal output from DMS neurons.

Effects of shifts in food deprivation on consummatory successive negative contrast

Rats exposed to a downshift from a large reward (32% sucrose) to a small reward (4% sucrose) show less consummatory behavior than unshifted rats always exposed to the small reward—an effect called consummatory successive negative contrast (cSNC). Four experiments studied the effects of shifts in deprivation level between preshift and postshift sessions on the size of the cSNC effect. This manipulation is designed to test the general proposition that the cSNC effect depends not only on external factors (e.g., reward disparity), but also on the internal state of the organism either at the time it first experiences the rewards (incentive learning), at the time of reward downshift (reward need), or as a function of the transition of states from pre- to postshift sessions (state dependency). Experiments 1–2 adjusted deprivation level during a 10-day interval between the last preshift and first postshift sessions. During this interval, food deprivation was either maintained or changed (increased or reduced) relative to preshift sessions. Experiments 3–4 maintained all animals at 81–85% of their ad lib weight during the entire experiment, but they were either fed before each session (nondeprivation condition) or fed after the session (deprivation condition). This procedure avoided the 10-day interval used in previous experiments. In three of the four experiments, the size of the cSNC effect increased when animals were deprived while exposed to the large reward (32% sucrose) during preshift sessions, independently of postshift deprivation conditions. The remaining experiment yielded inconclusive results. Of the three tested hypothesis, the incentive learning view received the strongest support. According to this view, the incentive value of the large reward is partly determined by the deprivation state of the organism at the time of learning.

Function of the centromedial amygdala in reward devaluation and open-field activity

The present research aimed at determining the role played by the amygdala in reward devaluation using transient inactivation induced by lidocaine microinfusions into the centromedial region. Two situations involving reward devaluation were tested in rats: consummatory successive negative contrast (cSNC) and anticipatory negative contrast (ANC). In cSNC, rats exposed to a downshift from 32% to 4% sucrose consume less 4% sucrose than rats always exposed to 4% sucrose. Extensive evidence suggests that reward devaluation in the cSNC situation is accompanied by negative emotion. In ANC, rats consume less 4% sucrose when each session is closely followed by access to 32% sucrose rather than by 4% sucrose. Evidence suggests that reward devaluation in the ANC situation does not involve negative emotions; rather, ANC appears to involve Pavlovian anticipation of the higher value solution. To test the effects of lidocaine microinfusions in a situation known to induce negative emotion, but unrelated to reward devaluation, animals were also exposed to a lighted open field. Centromedial amygdala inactivation reduced the cSNC effect and increased exploratory behavior in the open field, both effects consistent with a reduction in negative emotional state. However, no detectable effects of amygdala inactivation were observed in the ANC situation. These results suggest that, first, the function of the amygdala is not unique to reward devaluation and, second, it is concerned with tagging the devaluation experience with aversive valence.