Reinforcement Omission Research Articles

Reinforcement omission effects in rats with bilateral lesions in the substantia nigra pars compacta and ventral tegmental area

Reinforcement omission effects (ROEs) are characterized by higher response rates after reinforcement omission than after reinforcement delivery. This pattern of behavior is interpreted in terms of motivational and attentional processes. Recent studies from our laboratory have shown that the amygdala, nucleus accumbens, and medial prefrontal cortex are involved in ROE modulation. Also, the literature has demonstrated a role of other areas such as substantia nigra pars compacta (SNc) and the ventral tegmental area (VTA) in processes related to surprising events, such as prediction error and presentation or omission of an event (exteroceptive stimulus and reinforcement). Since these structures send projections to areas related to ROE modulation such as the amygdala, nucleus accumbens, and prefrontal cortex, the objective of the present study was to determine whether the SNc and VTA also integrate the circuit involved in ROE modulation. Rats were trained on a fixed-interval 12 s with limited-hold 6 s signaled schedule of reinforcement (Pre-lesion training). After acquisition of stable performance, the rats received bilateral neurotoxic lesions of the SNc (Experiment 1) and VTA (Experiment 2). Following postoperative recovery, the rats were submitted to two refresher sessions (Post-lesion training). Subsequently, the training was changed from a 100 to a 50% schedule of reinforcement (Post-lesion testing). In both experiments, the results showed that there was no difference in performance between sham rats and rats with bilateral lesions of the SNc or the VTA.

Novelty, Salience, and Surprise Timing Are Signaled by Neurons in the Basal Forebrain

The basal forebrain (BF) is a principal source of modulation of the neocortex [1-6] and is thought to regulate cognitive functions such as attention, motivation, and learning by broadcasting information about salience [2, 3, 5, 7-19]. However, events can be salient for multiple reasons-such as novelty, surprise, or reward prediction errors [20-24]-and to date, precisely which salience-related information the BF broadcasts is unclear. Here, we report that the primate BF contains at least two types of neurons that often process salient events in distinct manners: one with phasic burst responses to cues predicting salient events and one with ramping activity anticipating such events. Bursting neurons respond to cues that convey predictions about the magnitude, probability, and timing of primary reinforcements. They also burst to the reinforcement itself, particularly when it is unexpected. However, they do not have a selective response to reinforcement omission (the unexpected absence of an event). Thus, bursting neurons do not convey value-prediction errors but do signal surprise associated with external events. Indeed, they are not limited to processing primary reinforcement: they discriminate fully expected novel visual objects from familiar objects and respond to object-sequence violations. In contrast, ramping neurons predict the timing ofmany salient, novel, and surprising events. Their ramping activity is highly sensitive to the subjects' confidence in event timing and on average encodes the subjects' surprise after unexpected events occur. These data suggest that the primate BF contains mechanisms to anticipate the timing of a diverse set of important external events (via ramping activity) and to rapidly deploy cognitive resources when these events occur (via short latency bursting).

Large neurotoxic amygdala lesion impairs reinforcement omission effects

The amygdala has been implicated in a variety of motivational and attentional functions related to appetitive learning. Some studies showed that electrolytic lesions of the amygdaloid complex disrupted reinforcement omission effects (ROEs). However, recent studies that investigated ROEs employing neurotoxic lesions in specific amygdala areas - the central nucleus (CeA) or basolateral complex (BLA) of the amygdala - showed that CeA lesions or BLA lesions can interfere with, but do not eliminate ROEs. Although the effects of neurotoxic lesions in particular areas of the amygdala differed from those of a large gross lesion, these studies have indicated that it is possible that the amygdala is involved in ROE modulation. Furthermore, the effect that a neurotoxic lesion involving both areas (CeA and BLA) has on ROEs remains unexplored. Thus, the present study aimed to clarify whether the functional impairment related to large amygdala activation affects ROEs, in a neurotoxic lesion procedure. If this is the case, the underlying process may contribute to a better understanding of the involvement of the amygdala in ROEs modulation. After acquisition of stable performance during pre-lesion training in which rats were trained to respond on a fixed-interval 6 s with limited hold 6 s schedules (FI 6 s LH 6 s), lesions were made including both the CeA and BLA areas. In test sessions, the partial omission of reinforcement was introduced. The results showed that bilateral lesion of both CeA and BLA impaired ROEs, suggesting that amygdala is part of ROEs' modulation circuitry.

The Reinforcement Magnitude of Flavored Stimulus Interferes with Omission Effects in Rats

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.

Introduction to Special Issue on Incentive Relativity

In 1996, Charles Flaherty opened the prologue of his book Incentive Relativity with these words: “We compare. Many of the pleasures and irritations of life are related to the match between an event and our expectancies. We compare meals, composers, presidents, books, performances, salaries, and many other events that have some interest or value” (Flaherty, 1996, p. 1). The capacity of organisms to acquire reward expectations based on prior experience and to contrast them with their immediate reality is referred as incentive relativity. Incentive relativity implies not only a mechanism for processing information, but also an emotional component resulting from such comparison. Our passions, feelings, and emotions are often based on a comparison of relative outcomes, and, when such comparison results in what is appraised as a significant loss, a state of stress, anxiety, aggression, depression, and substance abuse can follow, among other psychopathological states. Almost two decades after Flaherty’s words, the analysis of incentive relativity effects continues to engage specialists in behavior, cognition, clinical psychology, pharmacology, and neuroscience. Nonhuman animals also compare incentives and exhibit affective responses to the outcome of such comparisons. This characteristic allows researchers coming from different disciplines to approach the scientific study of incentive relativity using animal models of human behavior. We now know a large variety of paradoxical learning effects based on the presentation of different reward values (contrast effects) or reward contingencies (partial reinforcement and extinction). The behavioral, environmental, hormonal, pharmacological, neurobiological, and genetic characterizations of these phenomena are part of a field of basic research of great tradition and, simultaneously, of current importance given their clinical and applied implications. In this special issue, leading experts review incentive relativity from a multidisciplinary perspective. Research on different approaches is presented, including empirical articles and critical reviews. A key focus of the present special issue is to highlight the contribution of animal research to extend our knowledge of some basic principles of learning and their emotional correlates in a variety of organisms, including humans. The first paper by Bueno, Judice-Daher, and Deliberato (pp. 410-419) investigates a phenomenon related to reward loss: the reinforcement omission effect. Bueno and co-authors aim to clarify the relationship between reinforcement magnitude and the reinforcement omission effect manipulating the magnitude linked to discriminative stimuli in a partial reinforcement fixed interval schedule. The empirical and theoretical implications of the results are discussed.

Prenatal ethanol increases sucrose reinforcement, an effect strengthened by postnatal association of ethanol and sucrose

Late prenatal exposure to ethanol recruits sensory processing of the drug and of its motivational properties, an experience that leads to heightened ethanol affinity. Recent studies indicate common sensory and neurobiological substrates between this drug and sweet tastants. Using a recently developed operant conditioning technique for infant rats, we examined the effects of prenatal ethanol history upon sucrose self-administration (postnatal days, PDs 14–17). Prior to the last conditioning session, a low (0.5 g/kg) or a high (2.5 g/kg) ethanol dose were paired with sucrose. The intention was to determine if ethanol would inflate or devalue the reinforcing capability of the tastant and if these effects are dependent upon prenatal ethanol history. Male and female pups prenatally exposed to ethanol (2.0 g/kg) responded more when reinforced with sucrose than pups lacking this antenatal experience. Independently of prenatal status, a low ethanol dose (0.5 g/kg) enhanced the reinforcing capability of sucrose while the highest dose (2.5 g/kg) seemed to ameliorate the motivational properties of the tastant. During extinction (PD 18), two factors were critical in determining persistence of responding despite reinforcement omission. Pups prenatally exposed to ethanol that subsequently experienced the low ethanol dose paired with sucrose, showed higher resistance to extinction. The effects here reported were not associated with differential blood alcohol levels across prenatal treatments. These results indicate that fetal ethanol experience promotes affinity for a natural sweet reinforcer and that low doses of ethanol are also capable of enhancing the positive motivational consequences of sucrose when ethanol and sucrose are paired during infancy.

Lesions of the orbitofrontal cortex do not affect the reinforcement omission effect in rats.

The reinforcement omission effect (ROE), reflected by response rates that are higher after reinforcement omission than after reinforcement delivery, has been attributed to both motivational and attentional consequences of the surprising reinforcement omission. These processes depend on the operation of separate amygdala areas and their connections with other brain systems. The interaction between the amygdala and orbitofrontal cortex has been suggested to be important in the modulation of motivational processes. The present study sought to verify whether the mechanisms involved in the ROE depend on the integrity of the orbitofrontal cortex. Prior to acquisition training, rats received bilateral excitotoxic lesions of the orbitofrontal cortex or sham lesions. Following postoperative recovery, the rats were trained on a fixed-interval 12 s limited-hold 6 s signaled schedule of reinforcement. After the acquisition of stable performance, the training was changed from a 100% to 50% schedule of reinforcement. The results showed that rats in both groups exhibited the ROE, with no differences in performance between groups following nonreinforcement. These data do not support the hypothesis that the orbitofrontal cortex is included in the neural substrates related to ROE modulation. The results also showed no difference in response rates between groups in the periods that preceded and followed nonreinforcement. These findings confirm previous studies that showed that the ROE is not related to the facilitation of behavior induced by nonreinforcement.

Lesions of the nucleus accumbens disrupt reinforcement omission effects in rats

The reinforcement omission effects (ROEs) have been attributed to both motivational and attentional consequences of the surprising reinforcement omission. Some studies have been showed amygdala is part of a circuit involved in the ROEs modulation. The view that amygdala lesions interfere with the ROEs is supported by evidence involving amygdala in responses correlated with motivational processes. These processes depend on the operation of separate amygdala areas and their connections with other brain systems. It has been suggested the interaction between the amygdala and the nucleus accumbens (NAC) is important to the modulation of motivational processes. Recent neuroimaging studies in human revealed reward delivery enhances activity of subcortical structures (NAC and amygdala), whereas reward omission reduces the activity in these same structures. The present study aimed to clarify whether the mechanisms related to ROEs depend on NAC. Prior to acquisition training, rats received bilateral excitotoxic lesions of NAC (NAC group) or sham lesions (Sham group). Following postoperative recovery, the rats were trained on a fixed-interval with limited hold signaled schedule of reinforcement. After acquisition of stable performance, the training was changed from 100% to 50% schedule of reinforcement. Both NAC and Sham groups presented the ROEs. However, after nonreinforcement, the response rates of the NAC group were lower than those registered in the Sham group. The performance of the NAC group decreased in the period following nonreinforcement when compared to the period preceding reinforcement omission. These findings suggest the NAC is part of the neural substrate involved in the ROEs modulation.

Role of the amygdala in the reinforcement omission effect.

The reinforcement omission effect (ROE) has been attributed to both motivational and attentional consequences of surprising reinforcement omission. Recent evidence suggests that the basolateral complex of the amygdala is involved in motivational components related to reinforcement value, whereas the central nucleus of the amygdala is involved in the processing of the attentional consequences of surprise. This study was designed to verify whether the mechanisms involved in the ROE depend on the integrity of either the basolateral amygdala complex or central nucleus of the amygdala. The ROE was evaluated in rats with lesions of either the central nucleus or basolateral complex of the amygdala and trained on a fixed-interval schedule procedure (Experiment 1) and fixed-interval with limited hold signaled schedule procedure (Experiment 2). The results of Experiment 1 showed that sham-operated rats and rats with lesions of either the central nucleus or basolateral area displayed the ROE. In contrast, in Experiment 2, subjects with lesions of the central nucleus or basolateral complex of the amygdala exhibited a smaller ROE compared with sham-operated subjects. Thus, the effects of selective lesions of amygdala subregions on the ROE in rats depended on the training procedure. Furthermore, the absence of differences between the lesioned groups in either experiment did not allow the dissociation of attentional or motivational components of the ROE with functions of specific areas of the amygdala. Thus, results did not show a functional double-dissociation between the central nucleus and basolateral area in the ROE.

Involvement of the basolateral complex and central nucleus of amygdala in the omission effects of different magnitudes of reinforcement

Evidence from appetitive Pavlovian and instrumental conditioning studies suggest that the amygdala is involved in modulation of responses correlated with motivational states, and therefore, to the modulation of processes probably underlying reinforcement omission effects. The present study aimed to clarify whether or not the mechanisms related to reinforcement omission effects of different magnitudes depend on basolateral complex and central nucleus of amygdala. Rats were trained on a fixed-interval 12s with limited hold 6s signaled schedule in which correct responses were always followed by one of two reinforcement magnitudes. Bilateral lesions of the basolateral complex and central nucleus were made after acquisition of stable performance. After postoperative recovery, the training was changed from 100% to 50% reinforcement schedules. The results showed that lesions of the basolateral complex and central nucleus did not eliminate or reduce, but interfere with reinforcement omission effects. The response from rats of both the basolateral complex and central nucleus lesioned group was higher relative to that of the rats of their respective sham-lesioned groups after reinforcement omission. Thus, the lesioned rats were more sensitive to the omission effect. Moreover, the basolateral complex lesions prevented the magnitude effect on reinforcement omission effects. Basolateral complex lesioned rats showed no differential performance following omission of larger and smaller reinforcement magnitude. Thus, the basolateral complex is involved in incentive processes relative to omission of different reinforcement magnitudes. Therefore, it is possible that reinforcement omission effects are modulated by brain circuitry which involves amygdala.

Influence of the reinforcement magnitude on omission effects

Reinforcement Omission Effects (ROEs), indicated by higher rate of responses after nonreinforced trials in a partial reinforcement schedule, have been interpreted as behavioral transient facilitation after nonreinforcement induced by primary frustration, and/or behavioral transient inhibition after reinforcement induced by demotivation or temporal control. The size of the ROEs should depend directly on the reinforcement magnitude. The present experiment aimed to clarify the relationship between reinforcement magnitude and the omission effects manipulating the magnitude linked to discriminative stimuli in a partial reinforcement FI schedule. The results showed that response rates were higher after omission than after reinforcement delivery. Besides, response rates were highest immediately after the reinforcement omission of a larger magnitude than of a smaller magnitude. These data are interpreted in terms of ROEs multiple process behavioral facilitation after nonreinforcement, and behavioral transient inhibition after reinforcement.

Prenatal methylmercury exposure increases responding under clocked and unclocked fixed interval schedules of reinforcement

Recent experiments have suggested that developmental methylmercury exposure produces perseverative behavior in adulthood. In the present experiment, interactions between developmental low-level methylmercury (MeHg) and nutritionally relevant dietary selenium (Se) on operant behavior and its persistence were examined in aged animals. Female rats were exposed, in utero, to 0, 0.5, or 5 ppm mercury as MeHg via drinking water, approximating mercury exposures of 0, 40, and 400 μg/kg/day. They also received both pre- and chronic post-natal exposure to a diet that was marginal (0.06 ppm) or rich (0.6 ppm) in Se, a nutrient believed to protect against MeHg's toxicity. This created a 2 (chronic Se) × 3 (gestational MeHg) full factorial design, with 6–8 female rats per cell. At eleven months of age, a multiple schedule consisting of alternating fixed interval (FI) and clocked FI (CFI) components was arranged. The CFI component was divided into 5, 24-second bins, each associated with a different auditory stimulus, providing a “clock.” Low and high response rates were evaluated using the initial 40% (bins 1 and 2) and last 20% (bin 5) of the FI and CFI components, respectively. Rats exposed to 5 ppm Hg made more responses than the other two groups during the last 20% of the intervals, regardless of selenium exposure or presence of the clock stimuli. They did not differ from the other groups during the initial 40% of the FI and CFI components. Following reinforcement omission for half of the intervals at 21 months of age, the 5 ppm Hg group continued to respond at higher rates than the other groups in both components.

Reinforcement omission in concurrent fixed-interval and random-interval schedules

The present experiment examined overall and local effects of omission of reinforcers in a choice situation. Pigeons' key-pecking responses were reinforced under concurrent fixed-interval and random-interval schedules of food presentation. After some weeks of baseline sessions in which the probability of reinforcement was 1.00, approximately 25% of food presentations from the fixed-interval schedule were omitted and replaced by timeout periods. In such omission sessions, the overall relative rates of responding to the fixed-interval schedule became lower than those in the baseline sessions. On the other hand, when relative rates of responding to the fixed-interval schedule in the omission sessions were calculated separately for fixed-interval cycles preceded by timeout periods and those preceded by food presentations, the relative rates in the former type of fixed-interval cycles were higher than those in the latter type for three out of four pigeons. These results mean that relative rates of responding cannot always be regarded as reflecting a relative value of an alternative, and that the overall effect of the omission of fixed-interval reinforcers is not reducible to the local effect of omission.

Temporal generalization accounts for response resurgence in the peak procedure

The peak interval (PI) procedure is commonly used to evaluate animals' ability to produce timed intervals. It consists of presenting fixed interval (FI) schedules in which some of the trials are replaced by extended non-reinforced trials. Responding will often resume (resurge) at the end of the non-reinforced trials unless precautions are taken to prevent it. Response resurgence was replicated in rats and pigeons. Variation of the durations of the FI and the non-reinforced probe trials showed it to be dependent on the time when reinforcement is expected. Timing of both the normal time to reinforcement, and the subsequent time to reinforcement during the probe trials followed Weber's law. A quantitative model of resurgence is described, suggesting how animals respond to the signaling properties of reinforcement omission. Model results were simulated using a stochastic binary counter.

Effects of breaks in the interval cycle on temporal tracking in pigeons

Two experiments examined the effects of inserting a break in a cyclic interval schedule on the temporal control of keypecking responses in pigeons. In Experiment 1, pigeons were exposed to intervals that changed from 45 to 15s and returned to 45 s. A break was inserted between the last 15-s and following 45-s interval and was in effect for either 0, 60, or 120 s. Either a blackout of lights in the test chamber or turning off the response key alone signaled breaks. In Experiment 2, we examined the effects of a wider range of breaks-0, 120, and 360 s. Post-reinforcement pause (PRP) tracked changes in the interval requirement across all conditions. However, breaks in the schedule, even one lasting 360 s, did not disrupt the overall time course of responding. The only effect that a break had on temporal performance was an elevation in the rate of responding and a shorter PRP in the interval following a break. The results suggest that breaks did not affect the birds' memory for short intervals, and that the momentary increase in responding may be related to the reinforcement omission effect.

Schedule-controlled behavior in rats exposed perinatally to the PCB mixture Aroclor 1254

Exposure to polychlorinated biphenyls (PCBs) has been shown to detrimentally affect learning and memory in children as well as schedule-controlled behavior in experimental animals. The objective of the present series of experiments was to extend research into the effects of PCBs on behavior maintained under both short (30 s) and long (5 min) fixed-interval (FI) schedules as well as an FI 3-min with reinforcement omission. Long–Evans rats were exposed to 0 or 6 mg/kg/day Aroclor 1254 (A1254) via oral gavage from Gestation Day 6 (GD 6) through Postnatal Day 21 (PND 21). At approximately PND 90, acquisition and steady-state performance were assessed under a series of FI reinforcement schedules consisting of FI 30-s, FI 5-min, and FI 3-min with 33% of the scheduled reinforcers omitted. Performance measures included index of curvature (IOC), response rate, and postreinforcement pause (PRP). There were no effects of A1254 on the acquisition of behavior under the FI 30-s schedule. Subsequently, there was an initial decrease in response rate and IOC and an increase in PRP following the transition from FI 30-s to the FI 5-min; there were, however, no treatment-related effects on any measure. During the reinforcement-omission procedure, there was an increase in the rate of responding and a decrease in IOC and PRP following omission intervals irrespective of treatment. These data are inconsistent with previous findings and suggest that perinatal A1254 exposure in the rat does not disrupt temporally organized behavior.

Time and memory: towards a pacemaker-free theory of interval timing.

A popular view of interval timing in animals is that it is driven by a discrete pacemaker-accumulator mechanism that yields a linear scale for encoded time. But these mechanisms are fundamentally at odds with the Weber law property of interval timing, and experiments that support linear encoded time can be interpreted in other ways. We argue that the dominant pacemaker-accumulator theory, scalar expectancy theory (SET), fails to explain some basic properties of operant behavior on interval-timing procedures and can only accommodate a number of discrepancies by modifications and elaborations that raise questions about the entire theory. We propose an alternative that is based on principles of memory dynamics derived from the multiple-time-scale (MTS) model of habituation. The MTS timing model can account for data from a wide variety of time-related experiments: proportional and Weber law temporal discrimination, transient as well as persistent effects of reinforcement omission and reinforcement magnitude, bisection, the discrimination of relative as well as absolute duration, and the choose-short effect and its analogue in number-discrimination experiments. Resemblances between timing and counting are an automatic consequence of the model. We also argue that the transient and persistent effects of drugs on time estimates can be interpreted as well within MTS theory as in SET. Recent real-time physiological data conform in surprising detail to the assumptions of the MTS habituation model. Comparisons between the two views suggest a number of novel experiments.

Extinction and reacquisition of differential responding in rats trained to discriminate between chlordiazepoxide and saline

In order to assess the resistance of drug discriminative responding to prolonged reinforcement omission, rats were trained to discriminate between either 6.0 mg/kg PO or 30.0 mg/kg PO. CDP and saline, using a food reinforced (V140-FR10) operant procedure. Dose generalization tests were conducted for both groups. Sessions were then run without reinforcement while drug (D) and saline (S) administrations were continued (extinction phase). After a maximum of 30 sessions without reinforcement, or when the rats emitted less than ten responses on either lever during three successive sessions (extinction criterion), reinforcement was reinstated. Finally, additional dose generalization tests with CDP were run. The discriminative responding controlled by the D and S administrations was not affected significantly by prolonged reinforcement omission in either group. For both groups, response rates were decreased and latencies to initiate responding were increased during the extinction phase. Response rate reduction occurred more rapidly for the drug condition in the high training dose group. This group also reached the extinction criterion sooner than the low training dose group. The reacquisition process occurred very rapidly. Response rates increased substantially after the first reinforcement had been obtained. After ten reacquisition sessions, response rates and latencies had reached values similar to those observed before extinction was initiated. Data revealed no differences between groups and the course of reacquisition did not differ between the S and D conditions.(ABSTRACT TRUNCATED AT 250 WORDS)

Signal properties of reinforcement and reinforcement omission on a multiple fixed-ratio schedule

A series of experiments used food-deprived pigeons to examine several parameters of reinforcement omission in an attempt to control changes of keypeck response measures on a subsequent schedule. In Experiments 1 and 2, the pigeons were tested with a multiple fixed-ratio schedule on which reinforcement was occasionally omitted at the completion of the first component. The duration of the delay occurring in lieu of reinforcement was systematically varied. In Experiment 3, the stimulus that signaled the second component of the schedule was altered to appear either more or less similar to the stimulus that signaled the first component. Two principal results are reported: (1) Response latency decreased and, to a much lesser extent, terminal response rate increased as the delay occurring in lieu of reinforcement decreased; and (2) both latency decrease and response-rate increase were enhanced by a second component stimulus which was similar to the first. The results are evaluated in terms of Amsel’s frustration theory and an analysis by Staddon which suggests that reinforcement inhibits responding. The data appear to support Staddon’s argument that rate increases and latency decreases following reinforcement omission are largely a function of an attenuation of the inhibitory influence of reinforcement, an effect that is enhanced by stimulus generalization. Accordingly, it is proposed that an animal’s response to reinforcement omission is determined by a stimulus complex that minimally includes the omission event and component cues.

The effects of lesions in amygdala or dorsomedial frontal cortex on reinforcement omission and noncontingent reinforcement in rats

Two groups of six rats with lesions of the amygdala or dorsomedial frontal cortex were compared to normal controls in their response to occasional omission of food reward following training on an FI 60-sec schedule (Experiment 1). Both brain-damaged groups showed reliably greater increases in their responding in intervals following reward omission compared to their responding in intervals following reward delivery than did controls. In a second experiment, there was no difference between these groups in their response to complete elimination of reward (extinction). However, both groups with lesions reliably reduced responding to a greater extent than did controls when rewards were delivered noncontingently (free) on an FI 60-sec schedule. The results of both experiments were interpreted as demonstrating a reduced efficacy of secondary reinforcers to control the behavior of subjects with these limbic lesions.