Multiple opioid receptors mediate feeding elicited by mu and delta opioid receptor subtype agonists in the nucleus accumbens shell in rats

Ragnauth, Andre; Moroz, Malgorzata; Bodnar, Richard J.

doi:10.1016/s0006-8993(00)02631-7

Cited by 63 publications

(50 citation statements)

References 51 publications

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“…Thus, nearly all regions of the medial shell appear able to cause dramatic increases in food intake in response to sufficient -opioid stimulation, consistent with previous reports (Ragnauth et al, 2000;Zhang and Kelley, 2000;Kim et al, 2004). The only medial shell region where DAMGO failed to increase eating was the farthest rostral 0.5 mm strip of medial shell, where neither dose evoked increased food intake above vehicle levels (anterior to ϩ2.0 bregma) (Figs.…”

Section: Experiments 2: Damgo Increases Food Intake Throughout the Medsupporting

confidence: 89%

“…Entire medial shell mediates opioid increase of food intake DAMGO throughout the entire shell increased food intake, confirming previous reports of wide nucleus accumbens distribution (Ragnauth et al, 2000;Zhang and Kelley, 2000;Kim et al, 2004). Food intake was more than quadrupled even at the caudal affective cold spot where DAMGO suppressed all affective reactions to tastes (Fig.…”

Section: Hedonic Function Maps: Coding and Causal Rolessupporting

confidence: 89%

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Hedonic Hot Spot in Nucleus Accumbens Shell: Where Do μ-Opioids Cause Increased Hedonic Impact of Sweetness?

Peciña¹,

Berridge²

2005

J. Neurosci.

593

493

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-Opioid systems in the medial shell of the nucleus accumbens contribute to hedonic impact ("liking") for sweetness, food, and drug rewards. But does the entire medial shell generate reward hedonic impact? Or is there a specific localized site for opioid enhancement of hedonic "liking" in the medial shell? And how does enhanced taste hedonic impact relate to opioid-stimulated increases in food intake? Here, we used a functional mapping procedure based on microinjection Fos plumes to localize opioid substrates in the medial shell of the nucleus accumbens that cause enhanced "liking" reactions to sweet pleasure and that stimulate food intake. We mapped changes in affective orofacial reactions of "liking"/"disliking" elicited by sucrose or quinine tastes after D-Ala 2 -N-Me-Phe 4 -Glycol 5-enkephalin (DAMGO) microinjections in rats and compared hedonic increases to food intake stimulated at the same sites. Our maps indicate that opioid-induced increases in sucrose hedonic impact are generated by a localized cubic millimeter site in a rostrodorsal region of the medial shell. In contrast, all regions of the medial shell generated DAMGO-induced robust increases in eating behavior and food intake. Thus, our results identify a locus for opioid amplification of hedonic impact and reveal a distinction between opioid mechanisms of food intake and hedonic impact. Opioid circuits for stimulating food intake are widely distributed, whereas hedonic "liking" circuits are more tightly localized in the rostromedial shell of the nucleus accumbens.

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Section: Experiments 2: Damgo Increases Food Intake Throughout the Medsupporting

confidence: 89%

Section: Hedonic Function Maps: Coding and Causal Rolessupporting

confidence: 89%

Hedonic Hot Spot in Nucleus Accumbens Shell: Where Do μ-Opioids Cause Increased Hedonic Impact of Sweetness?

Peciña¹,

Berridge²

2005

J. Neurosci.

593

493

View full text Add to dashboard Cite

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“…By contrast, the motivation to eat, expressed as higher food consumption, was increased by orexin at all sites throughout the entire medial shell. Widespread anatomical NAc stimulation of intake is also similar to mu-opioid stimulation, which increases eating at all sites throughout shell and core, as well as in dorsal and ventrolateral regions of neostriatum, in central nucleus of amygdala, and in medial prefrontal cortex (Castro and Berridge, 2014;DiFeliceantonio et al, 2012;Mahler and Berridge, 2009;Mena et al, 2011;Pecina and Berridge, 2005;Ragnauth et al, 2000;Richard et al, 2013;Thorpe and Kotz, 2005;Zhang and Kelley, 2000).…”

Section: Discussion Overviewmentioning

confidence: 94%

Orexin in Rostral Hotspot of Nucleus Accumbens Enhances Sucrose ‘Liking’ and Intake but Scopolamine in Caudal Shell Shifts ‘Liking’ Toward ‘Disgust’ and ‘Fear’

Castro

Terry

Berridge

2016

Neuropsychopharmacol

114

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The nucleus accumbens (NAc) contains a hedonic hotspot in the rostral half of medial shell, where opioid agonist microinjections are known to enhance positive hedonic orofacial reactions to the taste of sucrose ('liking' reactions). Within NAc shell, orexin/hypocretin also has been reported to stimulate food intake and is implicated in reward, whereas blockade of muscarinic acetylcholine receptors by scopolamine suppresses intake and may have anti-reward effects. Here, we show that NAc microinjection of orexin-A in medial shell amplifies the hedonic impact of sucrose taste, but only within the same anatomically rostral site, identical to the opioid hotspot. By comparison, at all sites throughout medial shell, orexin microinjections stimulated 'wanting' to eat, as reflected by increases in intake of palatable sweet chocolates. At NAc shell sites outside the hotspot, orexin selectively enhanced 'wanting' to eat without enhancing sweetness 'liking' reactions. In contrast, microinjections of the antagonist scopolamine at all sites in NAc shell suppressed sucrose 'liking' reactions as well as suppressing intake of palatable food. Conversely, scopolamine increased aversive 'disgust' reactions elicited by bitter quinine at all NAc shell sites. Finally, scopolamine microinjections localized to the caudal half of medial shell additionally generated a fearrelated anti-predator reaction of defensive treading and burying directed toward the corners of the transparent chamber. Together, these results confirm a rostral hotspot in NAc medial shell as a unique site for orexin induction of hedonic 'liking' enhancement, similar to opioid enhancement. They also reveal distinct roles for orexin and acetylcholine signals in NAc shell for hedonic reactions and motivated behaviors.

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“…Meilandt et al (2004) demonstrated that injections of FNA could depress MOR binding in the hippocampus after such injections by as much as 49% at 24 h, and decreases persisted for up to 11 days (Meilandt et al, 2004). This dose of FNA in the nucleus accumbens can also block the effects of DAMGO-induced feeding at 24 h (Ragnauth et al, 2000). Control rats received similar injections of the appropriate vehicle with each compound.…”

Section: Drugs and Microinjectionsmentioning

confidence: 95%

“…The MOR agonist DAMGO (0.5 mg/0.3 ml; Ragnauth et al, 2000;Hurley et al, 2003;Gonzalez-Nicolini et al, 2003) and the MOR antagonist CTAP (1 mg/0.3 ml; Gonzalez-Nicolini et al, 2003;Tang et al, 2005;Tershner and Helmstetter, 2000) were obtained from Sigma-Aldrich (St Louis, MO) and prepared in 0.9% sterile saline. The non-competitive MOR antagonist FNA (4 mg/0.3 ml; Ward et al, 1982Ward et al, , 1985Negus et al, 1993;Primeaux et al, 2006) was prepared in 15% cyclodextran-0.9% saline and was injected at least 24 h (plus maze) or 7 days (burying) before testing.…”

Section: Drugs and Microinjectionsmentioning

confidence: 99%

The Role of Amygdalar Mu-Opioid Receptors in Anxiety-Related Responses in Two Rat Models

Wilson

Junor

2008

Neuropsychopharmacol

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Amygdala opioids such as enkephalin appear to play some role in the control of anxiety and the anxiolytic effects of benzodiazepines, although the opioid receptor subtypes mediating such effects are unclear. This study compared the influences of mu-opioid receptor (MOR) activation in the central nucleus of the amygdala (CEA) on unconditioned fear or anxiety-like responses in two models, the elevated plus maze, and the defensive burying test. The role of MORs in the anxiolytic actions of the benzodiazepine agonist diazepam was also examined using both models.

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Multiple opioid receptors mediate feeding elicited by mu and delta opioid receptor subtype agonists in the nucleus accumbens shell in rats

Cited by 63 publications

References 51 publications

Hedonic Hot Spot in Nucleus Accumbens Shell: Where Do μ-Opioids Cause Increased Hedonic Impact of Sweetness?

Hedonic Hot Spot in Nucleus Accumbens Shell: Where Do μ-Opioids Cause Increased Hedonic Impact of Sweetness?

Orexin in Rostral Hotspot of Nucleus Accumbens Enhances Sucrose ‘Liking’ and Intake but Scopolamine in Caudal Shell Shifts ‘Liking’ Toward ‘Disgust’ and ‘Fear’

The Role of Amygdalar Mu-Opioid Receptors in Anxiety-Related Responses in Two Rat Models

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