Role of the amygdala in the reinforcement omission effect.

Psychology & Neuroscience

2013

Self Cite

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. Keywords: reinforcement omission effect, orbitofrontal cortex, operant behavior, rats.

Section: Discussionmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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

Judice-Daher

Psychology & Neuroscience

2013

Self Cite

“…After Training, in which animals demonstrated temporal expectancy for the reward in a FI 6 s LH 12 s schedule of reinforcement (Black et al, 1972;Judice-Daher et al, 2011, 2012Bueno et al, 2012;Tavares et al, 2014Tavares et al, , 2019, a session with temporal prediction error generated a memory updating of reward expectancy to a new temporal schedule. The prediction error, either due to the temporal change or to the omission of reward, increased in the BLA the activation of a protein (Arc) that is critical for memory formation.…”

Section: Discussionmentioning

confidence: 99%

Temporal prediction error triggers amygdala-dependent memory updating in appetitive operant conditioning in rats

Tavares

Front. Behav. Neurosci.

Doyère

2023

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Reinforcement learning theories postulate that prediction error, i.e., a discrepancy between the actual and expected outcomes, drives reconsolidation and new learning, inducing an updating of the initial memory. Pavlovian studies have shown that prediction error detection is a fundamental mechanism in triggering amygdala-dependent memory updating, where the temporal relationship between stimuli plays a critical role. However, in contrast to the well-established findings in aversive situations (e.g., fear conditioning), only few studies exist on prediction error in appetitive operant conditioning, and even less with regard to the role of temporal parameters. To explore if temporal prediction error in an appetitive operant paradigm could generate an updating and consequent reconsolidation and/or new learning of temporal association, we ran four experiments in adult male rats. Experiment 1 verified whether an unexpected delay in the time of reward’s availability (i.e., a negative temporal prediction error) in a single session produces an updating in long-term memory of temporal expectancy in an appetitive operant conditioning. Experiment 2 showed that negative prediction errors, either due to the temporal change or through reward omission, increased in the basolateral amygdala nucleus (BLA) the activation of a protein that is critical for memory formation. Experiment 3 revealed that the presence of a protein synthesis inhibitor (anisomycin) in the BLA during the session when the reward was delayed (Error session) affected the temporal updating. Finally, Experiment 4 showed that anisomycin, when infused immediately after the Error session, interfered with the long-term memory of the temporal updating. Together, our study demonstrated an involvement of BLA after a change in temporal and reward contingencies, and in the resulting updating in long-term memory in appetitive operant conditioning.

“…KA was infused with a 5 µL Hamilton syringe over a 2-min period according to the following coordinates: SNc (n=27): –4.3 mm posterior to bregma and 2.2 mm from the midline, with infusions to a depth of 7.4 mm from the skull surface (0.25 µL per site) (19). The Sham-SNc (n=16) groups received the same surgical treatment, with the exception that no solution was infused (7,8,10,11,20,21). After surgery, all rats received a single subcutaneous injection of 0.1 mL per 100 g body mass (2.15 mg/mL) of Flunixin Meglumine (Banamine®, 50 mg/mL, Intervet, Brazil) for pain relief and were allowed to recover from the surgery for 5–7 days before behavioral testing.…”

Section: Methodsmentioning

confidence: 99%

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

Tavares

Judice-Daher

2019

Braz J Med Biol Res

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.