General, μ and κ opioid antagonists in the nucleus accumbens alter food intake under deprivation, glucoprivic and palatable conditions

Bodnar, Richard J.; Glass, Michael J.; Ragnauth, Andre; Cooper, Madeline L.

doi:10.1016/0006-8993(95)00957-r

Cited by 115 publications

(80 citation statements)

References 69 publications

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“…Hence, the attenuation of EtOH self-administration in the present study particularly at the lower end of the dose response (0.5-10 mg) may be due, primarily to an action of nalmefene at m-opioid receptors. Similar conclusions have been reached by other investigators employing parenteral administration of nonselective opiate antagonists with humans, primates, and rodents (June et al, 1998Mason et al, 1994;Rodefer et al, 1999 While the results of the present study suggest that microinjection of nalmefene in the NACC and VTA may preferentially attenuate the reinforcing properties of EtOH when more than one reinforcer is presented concurrently, it is important to note that selective and nonselective opioid receptor antagonists differentially reduce various forms of caloric and noncaloric food intake following central administration (Beczkowska et al, 1993;Bodnar, 1996;Bodnar et al, 1995;Gosnell et al, 1986;Kelley et al, 1996;Ragnauth et al, 1997). However, because the saccharin solution in the present study was devoid of calories, the degree to which nalmefene preferentially attenuates motivated responding for caloric solutions when given concurrently with EtOH is not clear.…”

Section: Opioid Receptors In the Nacc Play A More Salient Role Than Vsupporting

confidence: 88%

“…These data suggest that given i.c.v., m antagonists are effective in reducing saccharin and sucrose intake, d1 receptors appear more salient in regulating saccharin reinforcement, while k-opioid receptors may be more important in mediating sucrose reinforcement. Others have reported that bilateral infusion of naltrexone and a mselective antagonist directly in the NACC reduce sucrose intake; however, d and k antagonists were ineffective (Bodnar et al, 1995;Kelley et al, 1996). Thus, naltrexone appears to suppress sucrose intake primarily due to blockade of m-opioid receptors.…”

Section: Opioid Receptors In the Nacc Play A More Salient Role Than Vmentioning

confidence: 99%

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Central Opioid Receptors Differentially Regulate the Nalmefene-Induced Suppression of Ethanol- and Saccharin-Reinforced Behaviors in Alcohol-Preferring (P) Rats

June

Cummings

Eiler

et al. 2003

Neuropsychopharmacol

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The exact opioid-sensitive receptors participating in EtOH-seeking behaviors remains unclear. Previous studies have reported higher densities of m-opioid receptor binding in the nucleus accumbens (NACC) of P relative to NP rats; however, no differences were seen in d-receptor binding. In contrast to the NACC, substantially lower levels of m-receptor binding have been observed in the ventral tegmental area (VTA) of both P and NP rats, albeit no line differences have been observed. In the present study, opioid receptors in the NACC, VTA, and hippocampus were evaluated for their capacity to regulate both EtOH-and saccharin-motivated behaviors in the genetically selected alcohol-preferring (P) rat. To accomplish this, nalmefene, an opiate antagonist with preferential binding affinity for the m-opioid receptor was unilaterally or bilaterally infused during concurrent availability of 1 h daily EtOH (10% v/v) and saccharin (0.025 or 0.050% w/v) solutions. Rats performed under a two-lever fixed ratio (FR) schedule in which four responses on one lever produced the EtOH solution, and four on a second lever produced the saccharin solution. The results demonstrated that when responding maintained by both EtOH and saccharin are matched at basal levels, unilateral (1-60 mg) or bilateral (0.5-10 mg) microinjections of nalmefene into the NACC produced selective dose-dependent reductions on responding maintained by EtOH. Unilateral (40, 60 mg) and bilateral (10 mg) VTA infusions were also observed to selectively reduced EtOH responding; however, greater nalmefene doses were required and the magnitude of suppression on EtOH responding was markedly less compared with the NACC. The greater sensitivity of nalmefene to suppress EtOH responding in the NACC is likely due to the greater number of opioid receptors in the NACC relative to the VTA. Only bilateral infusion of the 40 mg dose in the NACC and VTA suppressed responding maintained by both EtOH and saccharin. In contrast, intrahippocampal infusions dose dependently suppressed EtOH-and saccharin-maintained responding over a range of doses (1-20 mg). The present study provides evidence that nalmefene suppresses EtOH-motivated behaviors via blockade of opioid receptors within the NACC and VTA, and under various dose conditions both reinforcer and neuroanatomical specificity can be observed.

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Section: Opioid Receptors In the Nacc Play A More Salient Role Than Vsupporting

confidence: 88%

Section: Opioid Receptors In the Nacc Play A More Salient Role Than Vmentioning

confidence: 99%

Central Opioid Receptors Differentially Regulate the Nalmefene-Induced Suppression of Ethanol- and Saccharin-Reinforced Behaviors in Alcohol-Preferring (P) Rats

June

Cummings

Eiler

et al. 2003

Neuropsychopharmacol

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“…Conversely, -opioid antagonists at diverse sites in the nucleus accumbens suppress eating and intake, especially for palatable foods (Cooper and Higgs, 1994;Bodnar et al, 1995;Kelley et al, 1996;Levine and Billington, 1997).…”

Section: Introductionmentioning

confidence: 99%

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

Peciña¹,

Berridge²

2005

J. Neurosci.

584

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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“…The orexigenic effects of these treatments are evident particularly in settings using preferred foods for the test diet (e.g., 39, 94, 95), although consumption of standard chow is also enhanced (9, 72). Conversely, drugs that block ORs reduce food intake (11,16,41,49). This hypophagia may occur especially under conditions when opioid pathways are highly activated (53).…”

mentioning

confidence: 99%

An orexigenic role for μ-opioid receptors in the lateral parabrachial nucleus

Wilson

Nicklous

Aloyo

et al. 2003

American Journal of Physiology-Regulatory, Integrative and Comp

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. The pontine parabrachial nucleus (PBN) has been implicated in regulating ingestion and contains opioids that promote feeding elsewhere in the brain. We tested the actions of the selective -opioid receptor (-OR) agonist [D-Ala 2 ,N-Me-Phe 4 ,Gly 5 -ol]enkephalin (DAMGO) in the PBN on feeding in male rats with free access to food. Infusing DAMGO (0.5-4.0 nmol/0.5 l) into the lateral parabrachial region (LPBN) increased food intake. The hyperphagic effect was anatomically specific to infusions within the LPBN, dose and time related, and selective for ingestion of chow compared with (nonnutritive) kaolin. The nonselective opioid antagonist naloxone (0.1-10.0 nmol intra-PBN) antagonized DAMGO-induced feeding, with complete blockade by 1.0 nmol and no effect on baseline. The highly selective -opioid antagonist D-Phe-Cys-Trp-Arg-Thr-Pen-Thr-NH2 (CTAP; 1.0 nmol) also prevented this action of DAMGO, but the -antagonist nor-binaltorphimine did not. Naloxone and CTAP (10.0 nmol) decreased intake during scheduled feeding. Thus stimulating -ORs in the LPBN increases feeding, whereas antagonizing these sites inhibits feeding. Together, our results implicate -ORs in the LPBN in the normal regulation of food intake.feeding; hyperphagia; DAMGO; naloxone; CTAP STIMULATING ANY OF THE SUBTYPES of opioid receptors (ORs; , , ␦) or the related orphan receptor for nociceptin increases food intake in mammals (6,24,26,71,77). The orexigenic effects of these treatments are evident particularly in settings using preferred foods for the test diet (e.g., 39, 94, 95), although consumption of standard chow is also enhanced (9, 72). Conversely, drugs that block ORs reduce food intake (11,16,41,49). This hypophagia may occur especially under conditions when opioid pathways are highly activated (53). The data, therefore, suggest that opioid peptides play roles in the physiological control of feeding.The anatomic loci subserving opioidergic feeding are distributed widely throughout the brain. Attention has focused on the nucleus accumbens (NAC) and the rest of the ventral striatum as a critical region (9,72,94,95). Infusing opioid agonists into the ventral tegmental area of the midbrain, which projects onto the ventral striatum, also stimulates feeding (45, 67); this circuitry is consistent with the view assigning a broader role for opioids to support positive affect and appetitive reward (39, 70). Another (probably integrated) circuit is defined by observations that opioid stimulation of the paraventricular hypothalamic nucleus (21, 22) The parabrachial nucleus (PBN) of the pons has bidirectional communication with the PVN, central nucleus of the amygdala, and NTS (19,29,61,62). The multiple subnuclei of the PBN sort afferent input from second-order sensory neurons originating in the NTS and spinal cord (38,83) and distribute the information to rostral targets (19,36,37,68). This sensory processing includes neurotransmission underlying gustatory and visceral function and their convergence (8,30,38).It is logical, then, that the PBN has been imp...

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General, μ and κ opioid antagonists in the nucleus accumbens alter food intake under deprivation, glucoprivic and palatable conditions

Cited by 115 publications

References 69 publications

Central Opioid Receptors Differentially Regulate the Nalmefene-Induced Suppression of Ethanol- and Saccharin-Reinforced Behaviors in Alcohol-Preferring (P) Rats

Central Opioid Receptors Differentially Regulate the Nalmefene-Induced Suppression of Ethanol- and Saccharin-Reinforced Behaviors in Alcohol-Preferring (P) Rats

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

An orexigenic role for μ-opioid receptors in the lateral parabrachial nucleus

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