Emotional and behavioral correlates of the anterior cingulate cortex during associative learning in rats

Takenouchi, Kazunori; Nishijo, Hisao; Uwano, Teruko; Tamura, Ryoi; Takigawa, Morikuni; Ono, Taketoshi

doi:10.1016/s0306-4522(99)00216-x

Cited by 68 publications

(50 citation statements)

References 77 publications

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“…Conditioned stimuli generally produce decreases in the activity of neurons in the anterior cingulate cortex and the PrL regions, whether predictive of a natural food reward or an aversive footshock (Garcia et al, 1999;Takenouchi et al, 1999). Although there is no clear evidence that the direction of a change in gene expression is directly correlated with neuronal activity, the decrease in expression of ␥ PKC in medial prefrontal cortical regions in response to the cocaine-associated cue shown here may reflect a similar conditioned decrease in neuronal activity.…”

Section: Processing the Cs In The Medial Prefrontal Frontal Cortexmentioning

confidence: 66%

“…Anterior cingulate cortex lesions, but not mPFC lesions that encompass PrL cortex, disrupt Pavlovian stimulus-reward associations, whereas more rostral mPFC lesions result selectively in attentional deficits (Bussey et , 1997a,b). Moreover, rostral anterior frontal cortex neurons (encompassing the Cg1 region studied here) respond selectively to stimuli predictive of food reward (Takenouchi et al, 1999). In the context of addictive behavior, not only is the anterior cingulate cortex activated on exposure to cocaine cues, but selective lesions of the anterior cingulate or prelimbic cortices prevent the control over cocaine-seeking behavior by drug-associated cues (Weissenborn et al, 1997).…”

Section: Processing the Cs In The Medial Prefrontal Frontal Cortexmentioning

confidence: 99%

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Limbic-Cortical-Ventral Striatal Activation during Retrieval of a Discrete Cocaine-Associated Stimulus: A Cellular Imaging Study with γ Protein Kinase C Expression

Thomas

Everitt

2001

J. Neurosci.

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We investigated the neuronal activation associated with reexposure to a discrete cocaine-associated stimulus using in situ hybridization to quantify the expression of the plasticityregulated gene, ␥ protein kinase C (␥ PKC), in the limbiccortical-ventral striatal system. Groups of rats were trained to self-administer cocaine paired with a light stimulus (Paired) or paired with an auditory stimulus but also receiving light presentations yoked to those in the Paired group (Unpaired). Additional groups received noncontingent cocaine-light pairings (Pavlovian) or saline-light pairings (Saline) that were yoked to the Paired group. After acquisition of self-administration by the Paired and Unpaired groups, all groups had a 3 d drug-and training-free period before being reexposed to noncontingent presentations of the light conditioning stimulus during a 5 min test session in the training context. There were four major patterns of results for regional ␥ PKC expression 2 hr later. (1) Changes occurred only in groups in which the light was predictive of cocaine. (2) Increases were seen in the amygdala, but decreases were seen in the medial prefrontal cortex. (3) No changes were seen in the hippocampus. (4) Although changes were observed in the basal and central nuclei of the amygdala and the prelimbic cortex in both the Paired and Pavlovian groups, additional changes were observed in the nucleus accumbens core, lateral amygdala, and anterior cingulate cortex in the Pavlovian group. These results suggest not only that regionally selective alterations in ␥ PKC expression are an index of the retrieval of Pavlovian associations formed between a drug and a discrete stimulus, but also that a distinct neural circuitry may underlie Pavlovian stimulus-reward associations in cocaine-experienced rats.

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Section: Processing the Cs In The Medial Prefrontal Frontal Cortexmentioning

confidence: 66%

Section: Processing the Cs In The Medial Prefrontal Frontal Cortexmentioning

confidence: 99%

Limbic-Cortical-Ventral Striatal Activation during Retrieval of a Discrete Cocaine-Associated Stimulus: A Cellular Imaging Study with γ Protein Kinase C Expression

Thomas

Everitt

2001

J. Neurosci.

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“…The anterior cingulate cortex in the rat appears to be organized topographically, with rostral and ventral parts representing stimulus attributes that predict reward or no reward, and caudal and dorsal parts related to the execution of learned instrumental behaviors (Takenouchi et al, 1999). Importantly, dopaminergic input to the medial prefrontal cortex changes whenever presentation of a response-contingent food reward deviates from what the animal has come to expect (Richardson & Gratton, 1998).…”

Section: Learning In the Anterior Cingulate Cortexmentioning

confidence: 99%

The neural basis of human error processing: Reinforcement learning, dopamine, and the error-related negativity.

Holroyd¹,

Coles²

2002

Psychological Review

3,479

357

3,712

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The authors present a unified account of 2 neural systems concerned with the development and expression of adaptive behaviors: a mesencephalic dopamine system for reinforcement learning and a "generic" error-processing system associated with the anterior cingulate cortex. The existence of the error-processing system has been inferred from the error-related negativity (ERN), a component of the event-related brain potential elicited when human participants commit errors in reaction-time tasks. The authors propose that the ERN is generated when a negative reinforcement learning signal is conveyed to the anterior cingulate cortex via the mesencephalic dopamine system and that this signal is used by the anterior cingulate cortex to modify performance on the task at hand. They provide support for this proposal using both computational modeling and psychophysiological experimentation.Human beings learn from the consequences of their actions. Thorndike (1911Thorndike ( /1970 originally described this phenomenon with his law of effect, which made explicit the commonsense notion that actions that are followed by feelings of satisfaction are more likely to be generated again in the future, whereas actions that are followed by negative outcomes are less likely to reoccur. This fundamental reinforcement learning principle has been developed by the artificial intelligence community into a body of algorithms used to train autonomous systems to operate independently in complex and uncertain environments (Barto & Sutton, 1997;Sutton & Barto, 1998). Research has also evaluated the neural mechanisms underlying reinforcement learning in biological systems, but these mechanisms are still poorly understood.In this article, we provide a framework for understanding the neural basis of reinforcement learning in humans. Our proposal links together two areas of research that have, until now, been considered separately. On the one hand, we have previously inferred the existence of a generic, high-level error-processing system in humans from the error-related negativity (ERN), a negative deflection in the ongoing electroencephalogram (EEG) seen when human participants commit errors in a wide variety of psychological tasks. The ERN appears to be generated in the anterior cingulate cortex. On the other hand, other researchers have argued that the mesencephalic dopamine system conveys reinforcement learning signals to the basal ganglia and frontal cortex, where they are used to facilitate the development of adaptive motor programs. Although the reinforcement learning function attributed to the mesencephalic dopamine system and the error-processing function associated with the ERN appear to be concerned with the same problem-namely, evaluating the appropriateness of ongoing events, and using that information to facilitate the development and expression of adaptive behaviors-a possible relationship between these two systems remains to be explored.In this article, we propose a hypothesis that unifies the two accounts by explicitly linking the gen...

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“…Activity in the NAcc is increased during REM sleep (Lena et al 2005). Other reward-related regions, like the ventromedial PFC (Haber and Knutson 2010) and the ACC, which assign a positive or negative value to future outcomes (Bush et al 2002;Takenouchi et al 1999), are activated during REM sleep, in both animals and humans (Lena et al 2005;Maquet et al 1996Maquet et al , 2000. In addition, neuronal activity in the hippocampus displays a theta rhythm (i.e., an oscillatory pattern in EEG with a frequency range of 5-12 Hz in behaving rats and 4-7 Hz in humans) during REM sleep in both animals (Popa et al 2010;Winson 1972) and humans (Cantero et al 2003) studies.…”

Section: Activation Of Reward Networkmentioning

confidence: 99%

Sleep and Emotional Functions

Perogamvros

Schwartz

2013

Sleep, Neuronal Plasticity and Brain Function

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In this chapter, we review studies investigating the role of sleep in emotional functions. In particular, evidence has recently accumulated to show that brain regions involved in the processing of emotional and reward-related information are activated during sleep. We suggest that such activation of emotional and reward systems during sleep underlies the reprocessing and consolidation of memories with a high affective and motivational relevance for the organism. We also propose that these mechanisms occurring during sleep promote adapted cognitive and emotional responses in the waking state, including overnight performance improvement, creativity, and sexual functions. Activation across emotional-limbic circuits during sleep also appears to promote emotional maturation and the emergence of consciousness in the developing brain.

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Emotional and behavioral correlates of the anterior cingulate cortex during associative learning in rats

Cited by 68 publications

References 77 publications

Limbic-Cortical-Ventral Striatal Activation during Retrieval of a Discrete Cocaine-Associated Stimulus: A Cellular Imaging Study with γ Protein Kinase C Expression

Limbic-Cortical-Ventral Striatal Activation during Retrieval of a Discrete Cocaine-Associated Stimulus: A Cellular Imaging Study with γ Protein Kinase C Expression

The neural basis of human error processing: Reinforcement learning, dopamine, and the error-related negativity.

Sleep and Emotional Functions

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