Large Food Reward Research Articles

Effects of fentanyl self-administration on risk-taking behavior in male rats.

Individuals with opioid use disorder (OUD) exhibit impaired decisionmaking and elevated risk-taking behavior. In contrast to the effects of natural and semi-synthetic opioids, however, the impact of synthetic opioids on decisionmaking is still unknown. The objective of the current study was to determine how chronic exposure to the synthetic opioid fentanyl alters risk-based decisionmaking in adult male rats. Male rats underwent 14 days of intravenous fentanyl or oral sucrose self-administration. After 3 weeks of abstinence, rats were tested in a decision-making task in which they chose between a small, safe food reward and a large food reward accompanied by variable risk of footshock punishment. Following testing in the decision-making task, rats were tested in control assays that assessed willingness to work for food and shock reactivity. Lastly, rats were tested on a probabilistic reversal learning task to evaluate enduring effects of fentanyl on behavioral flexibility. Relative to rats in the sucrose group, rats in the fentanyl group displayed greater choice of the large, risky reward (risk taking), an effect that was present as long as 7 weeks into abstinence. This increased risktaking was driven by enhanced sensitivity to the large rewards and diminished sensitivity to punishment. The fentanyl-induced elevation in risktaking was not accompanied by alterations in food motivation or shock reactivity or impairments in behavioral flexibility. Results from the current study reveal that the synthetic opioid fentanyl leads to long-lasting increases in risktaking in male rats. Future experiments will extend this work to females and identify neural mechanisms that underlie these drug-induced changes in risktaking.

Effects of a high-fat diet on impulsive choice in rats

IntroductionObesity and binge eating disorder are associated with high levels of impulsivity, but the causal role of eating and palatable food in these associations is unclear. Studies in rodents show that a high-fat diet can increase one aspect of impulsivity (impulsive action); it is less clear, however, whether a dissociable aspect of impulsivity (impulsive choice) is similarly affected. Hence, the aim of this study was to ascertain whether chronic exposure to a high-fat diet would alter impulsive choice. MethodsMale rats were maintained on either a high-fat or control chow diet for two weeks ad libitum. They then underwent equi-caloric food restriction for the duration of the experiment, with each group maintained on their respective diet. To measure impulsive choice, rats were trained on a delay discounting task (DDT) in which they made discrete choices between a lever that delivered a small food reward immediately and a lever that delivered a large food reward accompanied by systematically increasing delays. Upon reaching stable performance on the DDT, rats were given acute systemic injections of amphetamine prior to testing in the DDT to determine whether increased monoamine transmission affected impulsive choice differently in the two diet groups. Lastly, subjects were tested on a progressive ratio schedule of reinforcement to assess motivation for a sucrose reward. ResultsThere was no significant effect of the high-fat diet on impulsive choice. Further, amphetamine decreased choice of the large, delayed reward (increased impulsive choice) to the same extent in both groups. Exposure to the high-fat diet did, however, increase motivation to obtain a sucrose reward. ConclusionsThese experiments reveal that, under conditions that do not promote weight gain, a chronic high-fat diet does not affect impulsive choice in a delay discounting task. The data are surprising in light of findings showing that this same diet alters impulsive action, and highlight the necessity of further research to elucidate relationships between palatable food consumption and impulsivity.

Regulation of risky decision making by gonadal hormones in males and females.

Psychiatric diseases characterized by dysregulated risky decision making are differentially represented in males and females. The factors that govern such sex differences, however, remain poorly understood. Using a task in which rats make discrete trial choices between a small, "safe" food reward and a large food reward accompanied by varying probabilities of footshock punishment, we recently showed that females are more risk averse than males. The objective of the current experiments was to test the extent to which these sex differences in risky decision making are mediated by gonadal hormones. Male and female rats were trained in the risky decision-making task, followed by ovariectomy (OVX), orchiectomy (ORX), or sham surgery. Rats were then retested in the task, under both baseline conditions and following administration of estradiol and/or testosterone. OVX increased choice of the large, risky reward (increased risky choice), an effect that was attenuated by estradiol administration. In contrast, ORX decreased risky choice, but testosterone administration was without effect in either ORX or sham males. Estradiol, however, decreased risky choice in both groups of males. Importantly, none of the effects of hormonal manipulation on risky choice were due to altered shock sensitivity or food motivation. These data show that gonadal hormones are required for maintaining sex-typical profiles of risk-taking behavior in both males and females, and that estradiol is sufficient to promote risk aversion in both sexes. The findings provide novel information about the mechanisms supporting sex differences in risk taking and may prove useful in understanding sex differences in the prevalence of psychiatric diseases associated with altered risk taking.

The perirhinal cortex supports spatial intertemporal choice stability.

In order to optimize outcomes in the face of uncertainty, one must recall past experiences and extrapolate to the future by assigning values to different choice outcomes. This behavior requires an interplay between memory and reward valuation, necessitating communication across many brain regions. At the anatomical nexus of this interplay is the perirhinal cortex (PRC). The PRC is densely connected to the amygdala and orbital frontal cortex, regions that have been implicated in reward-based decision making, as well as the hippocampus. Thus, the PRC could serve as a hub for integrating memory, reward, and prediction. The PRC's role in value-based decision making, however, has not been empirically examined. Therefore, we tested the role of the PRC in a spatial delay discounting task, which allows rats to choose between a 1-s delay for a small food reward and a variable delay for a large food reward, with the delay to the large reward increasing after choice of each large reward and decreasing after each small reward. The rat can therefore adjust the delay by consecutively choosing the same reward or stabilize the delay by alternating between sides. The latter has been shown to occur once the 'temporal cost' of the large reward is established and is a decision-making process termed 'exploitation'. When the PRC was bilaterally inactivated with the GABA(A) agonist muscimol, rats spent fewer trials successfully exploiting to maintain a fixed delay compared to the vehicle control condition. Moreover, PRC inactivation resulted in an increased number of vicarious trial and error (VTE) events at the choice point, where rats had to decide between the two rewards. These behavioral patterns suggest that the PRC is critical for maintaining stability in linking a choice to a reward outcome in the face of a variable cost.

Monoaminergic modulation of decision-making under risk of punishment in a rat model.

The ability to decide advantageously among options that vary in both their risks and rewards is critical for survival and well-being. Previous work shows that some forms of risky decision-making are robustly modulated by monoamine signaling, but it is less clear how monoamine signaling modulates decision-making under risk of explicit punishment. The goal of these experiments was to determine how this form of decision-making is modulated by dopamine, serotonin, and norepinephrine signaling, using a task in which rats choose between a small, 'safe' food reward and a large food reward associated with variable risks of punishment. Preference for the large, risky reward (risk-taking) was reduced by administration of a D2/3 dopamine receptor agonist (bromocriptine) and a selective D2 agonist (sumanirole). The selective D3 agonist PD128907 appeared to attenuate reward discrimination abilities but did not affect risk-taking per se. In contrast, drugs targeting serotonergic and noradrenergic signaling had few if any effects on choice behavior. These data suggest that in contrast to other forms of risky decision-making, decision-making under risk of punishment is selectively modulated by dopamine signaling, predominantly through D2 receptors.

Risky decision-making is associated with impulsive action and sensitivity to first-time nicotine exposure

Excessive risk-taking is common in multiple psychiatric conditions, including substance use disorders. The risky decision-making task (RDT) models addiction-relevant risk-taking in rats by measuring preference for a small food reward vs. a large food reward associated with systematically increasing risk of shock. Here, we examined the relationship between risk-taking in the RDT and multiple addiction-relevant phenotypes. Risk-taking was associated with elevated impulsive action, but not impulsive choice or habit formation. Furthermore, risk-taking predicted locomotor sensitivity to first-time nicotine exposure and resilience to nicotine-evoked anxiety. These data demonstrate that risk preference in the RDT predicts other traits associated with substance use disorder, and may have utility for identification of neurobiological and genetic biomarkers that engender addiction vulnerability.

Validation of a novel cognitive bias task based on difference in quantity of reinforcement for assessing environmental enrichment

Cognitive bias tasks purport to assess affective states via responses to ambiguous stimuli. We hypothesized that a novel cognitive bias task based on positive reinforcement using quantity differences would detect changes in affect in captive grizzly bears (Ursus arctos horribilis). We trained bears (n = 8) to respond differently (nose or paw touch) to two stimuli (light or dark gray cue cards), with responses counterbalanced across bears. The two cues signaled a small or large food reward, respectively. Responses to ambiguous probe stimuli (i.e., shades of gray) intermediate to the trained stimuli were classified as either 'optimistic,' appropriate for the larger reward, or 'pessimistic,' appropriate for the smaller reward. In Experiment 1, we explored the contrast in reward size necessary to detect a change in response across probe stimuli (large reward, 3 or 6 apple slices: small reward, 1 slice). We observed a change in response across probe stimuli, with no difference in response between reward-value groups, indicating that a contrast of 3:1 apple slices was sufficient to affect responses. In Experiment 2, we investigated cognitive bias after 2.1 h of exposure to enrichment items varying in attractiveness. Results were unaffected by enrichment type or time spent interacting with enrichments, indicating that the task failed to demonstrate criterion validity for comparing mood following exposure to different enrichment items. However, greater time spent pacing prior to testing was associated with 'optimistic' judgments. The data provide some support for use of cognitive bias tasks based on quantity differences in animal welfare assessments involving captive wildlife.

Individual differences in choice (in)flexibility but not impulsivity in the common marmoset: An automated, operant-behavior choice task

Individual differences in behavioural flexibility are a significant issue in human psychopathology as well as in its animal models. We aimed to investigate individual variations of operant-choice behaviour in the common marmoset (Callithrix jacchus), a small New World primate, using a new operant panel with two hand-poking holes. MethodsExperimental subjects (N=16) were presented with a choice between a Small & Soon (SS) vs a Large & Late (LL) food reward. After extensive training (31 daily sessions with no delay, during which a basal, large-reward preference developed), the delay before release of LL was progressively increased (from 0 to 60s, during 16 daily sessions; indifferent point at delay=9s). Subjects were classified as either “flexible” or “non-flexible”, respectively, based on a decrease (or not) in the preference for LL with increasing delays. Each subject was also classified as “maximizer” (or “non-maximizer”) based on capacity (or not) to maximize the food payoff as delay increased. ResultsUpon delays shorter than the indifferent point (<9s), none of the subjects showed a shift from LL to SS, denoting a lack of delay-induced, cognitive impulsivity. Individual differences only emerged upon delays longer than the indifferent point (>9s), when a preference shift could be interpreted as economically-driven. In general, a profile of few unrewarded hand-pokes in reaction to initial delays (i.e., a low motor impulsivity) and of clear-cut basal LL preference seemed to predict elevated flexibility of choices and better food payoff, which was typical of subjects classified as both “flexible & maximizer”. ConclusionThese results provide normative data on the marmosets, which can be used as a model for the investigation of 1) individual differences in behavioural flexibility, as well as 2) biological mechanisms rooted in our evolutionary history.

Effects of acute administration of nicotinic and muscarinic cholinergic agonists and antagonists on performance in different cost–benefit decision making tasks in rats

Alterations in cost-benefit decision making accompany numerous neuropsychiatric conditions, including schizophrenia, attention deficit hyperactivity disorder, and addiction. Central cholinergic systems have been linked to the etiology and/or treatment of many of these conditions, but little is known about the role of cholinergic signaling in cost-benefit decision making. The goal of these experiments was to determine how cholinergic signaling is involved in cost-benefit decision making, using a behavioral pharmacological approach. Male Long-Evans rats were trained in either "probability discounting" or "delay discounting" tasks, in which rats made discrete-trial choices between a small food reward and a large food reward associated with either varying probabilities of omission or varying delays to delivery, respectively. The effects of acute administration of different doses of nicotinic and muscarinic acetylcholine receptor agonists and antagonists were assessed in each task. In the probability discounting task, acute nicotine administration (1.0mg/kg) significantly increased choice of the large risky reward, and control experiments suggested that this was due to robust nicotine-induced impairments in behavioral flexibility. In the delay discounting task, the muscarinic antagonists scopolamine (0.03, 0.1, and 0.3mg/kg) and atropine (0.3mg/kg) both significantly increased choice of the small immediate reward. Neither mecamylamine nor oxotremorine produced reliable effects on either of the decision making tasks. These data suggest that cholinergic receptors play multiple roles in decision making contexts which include consideration of reward delay or probability. These roles should be considered when targeting these receptors for therapeutic purposes.

Self-administered cocaine causes long-lasting increases in impulsive choice in a delay discounting task.

Cocaine use is associated with high levels of impulsive choice (preference for immediate over delayed rewards), but it is not clear whether cocaine use causes elevated impulsive choice, or whether elevated impulsive choice is solely a predisposing factor for cocaine use. This study examined the effects of prior cocaine self-administration on rats performing a delay discounting task commonly used to measure impulsive choice. Male Long-Evans rats were implanted with intravenous catheters, and following recovery, were trained to self-administer 30 mg/kg/day cocaine HCl (approx. 0.5 mg/kg/infusion) for 14 consecutive days (a control group received yoked intravenous saline infusions). Following three weeks of withdrawal, all rats were food-restricted and began training on the delay discounting task in standard operant chambers. On each trial, rats were given a choice between two levers. A press on one lever delivered a small food reward immediately, and a press on the other delivered a large food reward after a variable delay period. Rats that self-administered cocaine displayed greater impulsive choice (enhanced preference for the small immediate over the large delayed reward, as reflected by shorter indifference points) compared to controls, but were no different from controls on a "probabilistic discounting" task in which they chose between small certain and large uncertain rewards. These data suggest that self-administered cocaine can cause lasting elevations in impulsive choice, and that the high levels of impulsive choice observed in human cocaine users may be due in part to long-term effects of cocaine on brain function.

Balancing Risk and Reward: A Rat Model of Risky Decision Making

We developed a behavioral task in rats to assess the influence of risk of punishment on decision-making. Male Long-Evans rats were given choices between pressing a lever to obtain a small, “safe” food reward and a large food reward associated with risk of punishment (footshock). Each test session consisted of 5 blocks of 10 choice trials, with punishment risk increasing with each consecutive block (0, 25, 50, 75, 100%). Preference for the large, “risky” reward declined with both increased probability and increased magnitude of punishment, and reward choice was not affected by the level of satiation or the order of risk presentation. Performance in this risky decision-making task was correlated with the degree to which the rats discounted the value of probabilistic rewards, but not delayed rewards. Finally, the acute effects of different doses of amphetamine and cocaine on risky decision-making were assessed. Systemic amphetamine administration caused a dose-dependent decrease in choice of the large risky reward (i.e. – it made rats more risk-averse). Cocaine did not cause a shift in reward choice, but instead impaired rats’ sensitivity to changes in punishment risk. These results should prove useful for investigating neuropsychiatric disorders in which risk taking is a prominent feature, such as attention deficit/hyperactivity disorder and addiction.

Clomipramine and selegiline: do they influence impulse control?

Anxiety disorders in dogs are often accompanied by loss of impulse control and can result in inappropriate behaviour such as destructiveness, excessive barking and aggression. The reduction of these undesirable actions is the focus of behaviour therapy. Clomipramine and selegiline have been approved for the treatment of separation anxiety in dogs, but there are anecdotal reports that they produce inconsistent therapeutic effect. Hence, the aim of this study was to verify the efficacy of clomipramine and selegiline for regulating impulse control by using a rat model based on the delay of reward procedure. The principle is that the animal has to decide between an immediate small food reward, normally preferred by impulsive animals, and a delayed large food reward. In this study, acute effects of clomipramine (0.3-10.0 mg/kg), selegiline (0.3-3.0 mg/kg), and diazepam (1.0-3.0 mg/kg) on the impulsive behaviour of two breeding lines of rats with different anxiety-related behaviour were investigated. Neither clomipramine nor selegiline had an effect on impulse control in either breeding line. However, motor activity was decreased by clomipramine and increased by selegiline. Diazepam led to an increase in impulsive behaviour of one rat line concomitant with an increase in motor activity. The results of this rat model for studying impulsive behaviour suggest that a single administration of selegiline and clomipramine has no influence on impulsive behaviour.

Neural correlates of the proximity and quantity of anticipated food rewards in the ventral striatum of domestic chicks

To identify the neuro-cognitive substrates of valuation and choice, we analysed the neural correlates of anticipated food rewards in the ventral striatum of freely behaving chicks. One-week-old chicks were trained in a color-discrimination task using four color cues (red, yellow, green and blue), each of which was associated with a different food reward. Choosing a red bead was immediately rewarded with a large amount of food, choosing a yellow bead resulted in an immediate-small food reward, and choosing a green bead resulted in a late-large food reward. We selected chicks that consistently chose a large and immediate food reward (red over yellow, and red over green), with the proximity of the food valued higher than the size of the food reward (yellow over green). Of the 47 neurons recorded from the ventral striatum of these chicks, 20 neurons selectively showed cue-period responses to cues associated with food rewards. Five of these 20 neurons responded differentially during the cue period according to the expected delay to reward, and were thus assumed to code for the proximity of the reward. Additionally, three other neurons responded to the quantity of the reward. Furthermore, in the post-operant delay period, many of these 20 neurons showed reward-related activities that were linked to the proximity or presence of the food reward. We therefore propose that impulsive choice and behavioral perseveration observed after lesions of the ventral striatum could be due to impaired anticipation of rewards in the cue and delay periods, respectively.

Ethanol induces impulsive-like responding in a delay-of-reward operant choice procedure: impulsivity predicts autoshaping.

Autoshaping conditioned responses (CRs) are reflexive and targeted motor responses expressed as a result of experience with reward. To evaluate the hypothesis that autoshaping may be a form of impulsive responding, within-subjects correlations between performance on autoshaping and impulsivity tasks were assessed in 15 Long-Evans hooded rats. Autoshaping procedures [insertion of retractable lever conditioned stimulus (CS) followed by the response-independent delivery of food (US)] were followed by testing for impulsive-like responding in a two-choice lever-press operant delay-of-reward procedure (immediate small food reward versus delayed large food reward). Delay-of-reward functions revealed two distinct subject populations. Subjects in the Sensitive group (n=7) were more impulsive-like, increasing immediate reward choices at longer delays for large reward, while those in the Insensitive group (n=8) responded predominantly on only one lever. During the prior autoshaping phase, the Sensitive group had performed more autoshaping CRs, and correlations revealed that impulsive subjects acquired the autoshaping CR in fewer trials. In the Sensitive group, acute injections of ethanol (0, 0.25, 0.50, 1.00, 1.50 g/kg) given immediately before delay-of-reward sessions yielded an inverted U-shaped dose-response curve with increased impulsivity induced by the 0.25, 0.50, and 1.00 g/kg doses of ethanol, while choice strategy of the Insensitive group was not influenced by ethanol dose. Ethanol induced impulsive-like responding only in rats that were flexible in their response strategy (Sensitive group), and this group also performed more autoshaping CRs. Data support the hypothesis that autoshaping and impulsivity are linked.

Ibotenic acid lesions of the amygdala basolateral complex or central nucleus differentially effect the response to reductions in reward

The present study examined the role of the amygdala in the acquisition and expression of the Crespi effect (Crespi, L.P., Quantitative variation in incentive and performance in the white rat, Am. J. Psychol., 55 (1942) 467–517), also known as successive negative behavioral contrast. In Experiment One rats with bilateral amygdala cannulae were trained to run a straight alley for either a large (ten pellet) or small (one pellet) food reward. After 8 days of training, half of the rats in each reward condition received vehicle or ibotenic acid administered bilaterally into the amygdala. After 4 days of recovery from the induction of the lesions, training resumed. On Day 12 of training, the reward for rats in the large reward condition was shifted to one pellet and this reward level was maintained for the next 4 days of training. Both the lesioned and unlesioned shifted rats exhibited increased latencies to the reduction. However, shifted lesioned rats displayed a more persistent increase in latencies than shifted unlesioned rats, exhibiting significantly longer latencies than those of unlesioned rats by Day 15. This finding suggests that large amygdala lesions may impair learning of the appetitive value of the small reward. Experiment Two examined the effects of discrete ibotenic acid lesions of either the central nucleus or basolateral/lateral complex of the amygdala. Lesions of the central nucleus produced results similar to those of Experiment One. However, in Experiment Two the performance of shifted unlesioned and lesioned groups diverged significantly 1 day earlier, on Day 14. In contrast, lesions of the basolateral/lateral complex reduced the duration of the contrast effect. Shifted lesioned rats exhibited significantly lower latencies than shifted unlesioned rats by the first postshift day, Day 13. This finding suggests that the basolateral/lateral complex may be involved in learning about, or expressing the response to, the aversiveness of reward reduction.

The amygdala modulates memory for changes in reward magnitude: involvement of the amygdaloid GABAergic system

Rats with bilateral amygdala cannulae were trained to run a straight alley for a large or small food reward. Muscimol (MUS), a GABA A agonist, or bicuculline methiodide (BMI), a GABA A antagonist, were infused into the amygdala immediately after a reward shift. In Experiment 1, rats in the large-reward group were shifted to the small reward and immediately after received an infusion of vehicle or MUS bilaterally into the amygdala. The runway latencies of the shifted vehicle animals were increased in comparison with those of the unshifted controls. In contrast, the shifted MUS (0.001 nM, but not 0.01 nM) animals displayed latencies that were comparable to those of unshifted animals by the second postshift day. These findings suggest that muscimol dose-dependently attenuated the memory of the reward reduction. In Experiment 2 rats were trained as before except they received bilateral infusions of BMI into the amygdala immediately after reward reduction. The shifted BMI (0.1 nM, but not 0.3 nM) animals displayed increased runway latencies, in comparison with those of shifted vehicle animals, by the second postshift day. These findings suggest that BMI dose-dependently enhanced memory of the reward reduction. In Experiment 3, animals were trained as before except they first experienced a reward increase before receiving post-training injections of vehicle, MUS (0.001 nM) or BMI (0.1 nM). On the next day the reward was reduced. Despite reward reduction, shifted BMI animals persisted displaying low latencies for more trials than did shifted MUS animals. These findings suggest that BMI enhanced memory for the reward increase. More generally, the findings suggest that the amygdala and its GABAergic system is involved in memory consolidation for both positive and negative affective experiences.

The post-feeding responses of sows to the daily presentation of food rewards in a test arena

It has been suggested that feeding motivation and feeding behaviour are causally related to the performance of persistent oral behaviour in pigs. However, in a previous experiment we showed that the presentation of small food rewards to chronically food-restricted sows in a test arena did not elicit the performance of persistent feeding-like behaviours. In this paper we tested the hypothesis that the arousal generated by the expectation of a daily presentation of a food reward would be ‘channelled’ by a restrictive environment into the expression of persistent feeding-like behaviour. A 2 × 2 factorial design was used, in which sows were presented with either a 1 kg or an 18 g food reward (expected to engender different levels of arousal) in a 16 m 2 or 4 m 2 sand-bedded test pen during a 40 min observation period, each day for 26 days. It was shown that sows receiving the large food reward stood for a greater proportion of the time after food reward consumption than the sows receiving the small food reward (0.86 vs. 0.66 for the 1 kg and 18 g food reward, respectively; P < 0.05). Neither pen nor food reward size affected chewing behaviour or sand-directed behaviour ( P > 0.05). The proportion of time spent chewing increased with test day (0.15 vs. 0.36 for test day 1 and day 26, respectively; P < 0.01) but was independent of the arousal elicited by the large food reward and not affected by pen size. It appears that feeding motivation is not as closely related to the performance of persistent oral behaviours as had previously been thought. The ‘emotional state’ of the animal around feeding may be an important factor, and chronic food restriction may contribute to this state.

Muscimol Induces Retrograde Amnesia for Changes in Reward Magnitude

These experiments examined the effect of the GABAA, agonist, muscimol (MUS), on memory for changes in reward magnitude. In Experiment 1 rats were trained to run a straight alley for either a large or small food reward. After reaching asymptotic performance rats in the high reward group were shifted to the small food reward. Half the animals received 1.0 or 3.0 mg/kg (ip) of MUS or the equivalent volume of saline immediately after training. Shifted training continued for 3 more days and no further injections were given. Shifted saline animals displayed an increase in response latencies compared to unshifted controls with a sharp peak on the day after the shift. Shifted MUS receiving 1.0 mg/kg performed comparably to shifted saline animals. In contrast, shifted MUS animals receiving 3.0 mg/kg displayed performance comparable to shifted saline animals on the day of the shift but displayed a sharp increase in response latencies on the second day after the shift. These findings indicate that post-training systemic MUS injections delay the peak increase in response latencies and suggest that MUS induces retrograde amnesia for reward reduction. Experiment 2 examined the effect of MUS on the memory of a reward increase. Rats were first trained as in Experiment 1 and rats under the high reward condition were then shifted to the small reward. On the next training session, the large food reward was reinstated. Immediately after the session all animals were injected with saline or 3.0 mg/kg of MUS. The large food reward was continued for the remainder of training and no further injections were given. On the following session, the performance of the shifted saline animals was comparable to that of the unshifted controls while shifted MUS animals displayed significantly higher response latencies. The findings that MUS prevented the reduction in response latencies seen in saline-injected animals suggest that MUS also induces retrograde amnesia for reward increases.

Midazolam administered to rats induces anterograde amnesia for changes in reward magnitude.

L. P. Crespi (1942) showed that rats trained to run an alley for a large food reward slowed down when shifted to a small reward. This effect is usually interpreted as an aversive emotional response to reward reduction (A. Amsel, 1958). Benzodiazepines attenuate the behavioral effects of reward reduction (cf. C. F. Flaherty, 1990), but the emphasis has been on their anxiolytic, not memory-impairing, effects. Researchers trained rats (175-200 g) to run an alley for food until asymptote was reached. Reward magnitude was then either decreased (Experiment 1) or increased (Experiment 2). The benzodiazepine midazolam (1 mg/kg ip), injected immediately prior to a decrease or increase in reward magnitude, impaired the later retention of both changes in a manner consistent with anterograde amnesia. The findings suggest that the memory-impairing effects of benzodiazepines may, at least in part, influence the response to reward reduction.

Reward reductions found more aversive by rats fed environmentally contaminated salmon

Pacific salmon stocked in Lake Ontario concentrate persistent toxic chemicals such as PCBs, DDT, DDE, mercury and dioxin. The present experiments support earlier findings that consumption of these salmon by laboratory rats increases their behavioral reactions to negative events. For 20 days rats were fed a diet consisting of 30% Lake Ontario salmon or a control diet of Pacific Ocean salmon or no salmon. They were then trained to run down an alley to receive a large 15-pellet or small 1-pellet food reward (6 trials/day). Following 72 trials the 15-pellet groups were shifted to 1 pellet for 90 trials, and showed a contrast (depression) effect: they ran more slowly than the groups always given 1 pellet. Rats previously fed Lake Ontario salmon showed a much larger contrast effect than the two control groups. These results were replicated in a second experiment, and a group fed a 10% diet of Lake Ontario salmon for 60 days showed the same size contrast effect as the group fed a 30% diet for 20 days.