Opioid Limbic Circuit for Reward: Interaction between Hedonic Hotspots of Nucleus Accumbens and Ventral Pallidum

Smith, Ken G.; Berridge, Kent

doi:10.1523/jneurosci.4205-06.2007

Cited by 401 publications

(332 citation statements)

References 61 publications

(88 reference statements)

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“…Nalmefene may have blunted binge-like eating by blocking opioid receptors in the ventral tegmental area, thereby disinhibiting GABAergic inhibitory interneurons that synapse on dopamine neurons and decreasing dopamine release in the shell of the nucleus accumbens (Taber et al, 1998;MacDonald et al, 2003MacDonald et al, , 2004. Nalmefene also might have acted by blocking m-opioid receptors in the nucleus accumbens shell or ventral pallidum (Woolley et al, 2006;Ward et al, 2006), cooperative components of a neurocircuit for amplifying appetitive responses to preferred foods, substances of abuse, and other rewards (Smith and Berridge, 2007;Kelley et al, 2005).…”

Section: Discussionmentioning

confidence: 99%

Opioid-Dependent Anticipatory Negative Contrast and Binge-Like Eating in Rats with Limited Access to Highly Preferred Food

Cottone

Sabino

Steardo

et al. 2007

Neuropsychopharmacol

137

149

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Binge eating and an increased role for palatability in determining food intake are abnormal adaptations in feeding behavior linked to eating disorders and body weight dysregulation. The present study tested the hypothesis that rats with limited access to highly preferred food would develop analogous opioid-dependent learned adaptations in feeding behavior, with associated changes in metabolism and anxiety-like behavior. For this purpose, adolescent female Wistar rats were daily food deprived (2 h) and then offered 10-min access to a feeder containing chow followed sequentially by 10-min access to a different feeder containing either chow (chow/chow; n ¼ 7) or a highly preferred, but macronutrient-comparable, sucrose-rich diet (chow/preferred; n ¼ 8). Chow/preferred-fed rats developed binge-like hyperphagia of preferred diet from the second feeder and anticipatory chow hypophagia from the first feeder with a time course suggesting associative learning. The feeding adaptations were dissociable in onset, across individuals, and in their dose-response to the opioid-receptor antagonist nalmefene, suggesting that they represent distinct palatability-motivated processes. Chow/preferred-fed rats showed increased anxiety-like behavior in relation to their propensity to binge as well as increased feed efficiency, body weight, and visceral adiposity. Chow/preferred-fed rats also had increased circulating leptin levels and decreased growth hormone and 'active' ghrelin levels. Thus, the short-term control of food intake in rats with restricted access to highly preferred foods comes to rely more on hedonic, rather than nutritional, properties of food, through associative learning mechanisms. Such rats show changes in ingestive, metabolic, endocrine, and anxiety-related measures, which resemble features of binge eating disorders or obesity.

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Section: Discussionmentioning

confidence: 99%

Opioid-Dependent Anticipatory Negative Contrast and Binge-Like Eating in Rats with Limited Access to Highly Preferred Food

Cottone

Sabino

Steardo

et al. 2007

Neuropsychopharmacol

137

149

View full text Add to dashboard Cite

show abstract

“…It, like the VS, is an area of focus in the study of addictive behaviors (Mitrovic and Napier, 2002;Smith and Berridge, 2007;Tindell et al, 2006). The term VP was first used to describe, in rats, the forebrain region below the anterior commissure, extending into the anterior perforated space that contained pallidal-like cells.…”

Section: Ventral Pallidum (Figure 8)mentioning

confidence: 99%

The Reward Circuit: Linking Primate Anatomy and Human Imaging

Haber

Knutson

2009

Neuropsychopharmacol

3,180

193

2,859

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Although cells in many brain regions respond to reward, the cortical-basal ganglia circuit is at the heart of the reward system. The key structures in this network are the anterior cingulate cortex, the orbital prefrontal cortex, the ventral striatum, the ventral pallidum, and the midbrain dopamine neurons. In addition, other structures, including the dorsal prefrontal cortex, amygdala, hippocampus, thalamus, and lateral habenular nucleus, and specific brainstem structures such as the pedunculopontine nucleus, and the raphe nucleus, are key components in regulating the reward circuit. Connectivity between these areas forms a complex neural network that mediates different aspects of reward processing. Advances in neuroimaging techniques allow better spatial and temporal resolution. These studies now demonstrate that human functional and structural imaging results map increasingly close to primate anatomy.

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“…There is a special need for better understanding of how pleasure is generated by brain systems, and so we will focus particularly on pleasure in this paper. Smith et al (2008), based on Kringelbach (2005), Peciña et al (2006), and Smith and Berridge (2007) From sensation to pleasure Pleasure is never merely a sensation (Frijda 2007;Kringelbach and Berridge 2008;Ryle 1954). Instead, it always requires the activity of hedonic brain systems to paint an additional "hedonic gloss" onto a sensation to make it 'liked'.…”

Section: Multiple Psychological Components Of Rewardmentioning

confidence: 99%

“…For example, enhanced 'liking' reactions are not amplified 'in vacuum' as motor reactions by accumbens or pallidal activation but rather only if a palatable taste is also presented simultaneously, and always in a signature hedonic pattern of several 'liking' reactions. Hotspot enhancement of 'liking' never amplifies negative 'disliking' or neutral reactions, ruling out general activation explanations of increased hedonic reactions (Berridge 2000;Mahler et al 2007;Peciña and Berridge 2005;Smith and Berridge 2007). Also, converging evidence comes from studies of the neuronal coding of natural pleasure enhancements within hedonic hotspots Kringelbach 2005).…”

Section: Pleasure Generators: Hedonic Hotspots In the Brainmentioning

confidence: 99%

Affective neuroscience of pleasure: reward in humans and animals

2008

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Introduction Pleasure and reward are generated by brain circuits that are largely shared between humans and other animals. Discussion Here, we survey some fundamental topics regarding pleasure mechanisms and explicitly compare humans and animals. Conclusion Topics surveyed include liking, wanting, and learning components of reward; brain coding versus brain causing of reward; subjective pleasure versus objective hedonic reactions; roles of orbitofrontal cortex and related cortex regions; subcortical hedonic hotspots for pleasure generation; reappraisals of dopamine and pleasure-electrode controversies; and the relation of pleasure to happiness.

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Opioid Limbic Circuit for Reward: Interaction between Hedonic Hotspots of Nucleus Accumbens and Ventral Pallidum

Cited by 401 publications

References 61 publications

Opioid-Dependent Anticipatory Negative Contrast and Binge-Like Eating in Rats with Limited Access to Highly Preferred Food

Opioid-Dependent Anticipatory Negative Contrast and Binge-Like Eating in Rats with Limited Access to Highly Preferred Food

The Reward Circuit: Linking Primate Anatomy and Human Imaging

Affective neuroscience of pleasure: reward in humans and animals

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