Opiate blockade inhibits saccharin intake and blocks normal preference acquisition

Lynch, Wesley C.

doi:10.1016/0091-3057(86)90420-x

Cited by 112 publications

(33 citation statements)

References 16 publications

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“…In our study, it is unlikely that taste aversion is responsible for the observed decrease in consumption since the maximum dose was 1 mg/kg. In addition, other authors have shown that naloxone induced conditioned taste aversion only at high doses, while anorectic effects of naloxone are observed with doses much lower (Hunt et al, 1983;Leshem, 1984;Lynch, 1986). On the whole, our data are in accordance with the hypothesis that the opioid system regulates feeding through the modulation of the perception of food palatability.…”

Section: Discussionsupporting

confidence: 92%

“…Similar results were observed in rats given unrestricted access to sucrose or saccharin solutions or sweet chow (Cleary et al, 1996;Levine et al, 1995;Lynch, 1986). In humans, naltrexone (an opioid receptor antagonist) administration decreases the pleasantness of the food, without affecting the rated appetite prior meal initiation Gray, 1997, 2002).…”

Section: Discussionmentioning

confidence: 53%

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Differential Regulation of the Consummatory, Motivational and Anticipatory Aspects of Feeding Behavior by Dopaminergic and Opioidergic Drugs

Barbano

Cador

2005

Neuropsychopharmacol

114

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Various aspects of feeding behavior (eg consumption, motivation and anticipation) are regulated by homeostatic and hedonic systems, and are modulated by dopaminergic and opioid brain systems. Here, we have studied the modulation of these aspects of feeding behavior by opioid and dopaminergic neurotransmission while taking into account food palatability and homeostatic state. Foods that varied in palatability were presented to either food sated or food restricted rats following injections of different doses of naloxone, an opioid receptor antagonist, or flupenthixol, a dopaminergic receptor antagonist, in behavioral paradigms that measured different aspects of feeding. Naloxone decreased food intake in a dose-dependent manner in sated rats given access to palatable food, without modifying food intake in food restricted rats. Flupenthixol did not have any effect on food intake. With regard to motivation, which was tested in a straight alley, naloxone increased the latency to reach the food only in sated rats presented with palatable food. Flupenthixol did not modify the latency of any group. Conditioned locomotor activity to repeated food presentation, a measure of anticipation, is expressed only in food restricted rats. Naloxone did not modify anticipatory activity, whereas flupenthixol decreased it only in food restricted rats presented with palatable food. These results reinforce the idea that the opioid system regulates feeding through the modulation of the perceived palatability of food. The dopaminergic system seems to be more important for the regulation of anticipatory activity related to motivationally relevant stimuli.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 53%

Differential Regulation of the Consummatory, Motivational and Anticipatory Aspects of Feeding Behavior by Dopaminergic and Opioidergic Drugs

Barbano

Cador

2005

Neuropsychopharmacol

114

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“…One possibility is that opioids mediate the rewarding or palatable aspects of feeding. Thus, the ability of opioid antagonists to suppress intake is greater when palatable food items (lard or diets sweetened with sucrose) or drink are offered (Giraudo et al, 1993;Levine et al, 1982Levine et al, , 1995Lynch, 1986). Hypothalamic dynorphin A1-17 and prodynorphin mRNA levels are elevated by feeding a palatable diet rich in fat and sucrose whereas caloric restriction of the same diet decreases mRNA levels of prodynorphin, proenkephalin and POMC, as well as levels of dynorphin A1-17 (Welch et al, 1996).…”

Section: Discussionmentioning

confidence: 98%

Reduced alcohol consumption in mice lacking preprodynorphin

Blednov

Walker

Martinez

et al. 2006

Alcohol

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Many studies suggest a role for endogenous opioid peptides and their receptors in regulation of ethanol intake. It is commonly accepted that the κ-opioid receptors and their endogenous ligands, dynorphins, produce a dysphoric state and therefore may be responsible for avoidance of alcohol. We used mutant mice lacking preprodynorphin in a variety of behavioral tests of alcohol actions. Null mutant female, but not male, mice showed significantly lower preference for alcohol and consumed lower amounts of alcohol in a two-bottle choice test as compared with wild-type littermates. In the same test, knockout mice of both sexes showed a strong reduction of preference for saccharin compared to control mice. In contrast, under conditions of limited (4 hours) access (light phase of the light/dark cycle), null mutant mice did not show any differences in consumption of saccharin but they showed significantly reduced intake of sucrose. To determine the possible cause for reduction of ethanol preference and intake, we studied other ethanol-related behaviors in mice lacking the preprodynorphin gene. There were no differences between null mutant and wild type mice in ethanol-induced loss of righting reflex, acute ethanol withdrawal, ethanol-induced conditioned place preference or conditioned taste aversion to ethanol. These results indicate that deletion of preprodynorphin leads to substantial reduction of alcohol intake in female mice, and suggest thath this is caused by decreased orosensory reward of alcohol (sweet taste and/or palatability).

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“…More recently, Ookuma and colleagues have provided additional support for the involvement of a K-opioid pathway by showing that the K-antagonist nor-BNI would mimic the effects of enterostatin and that subthreshold doses of nor-BNI and enterostatin, when combined, reduce fat intake (57). Opiates are recognized to have an important role in preference acquisition (43).…”

Section: Central Effects Of Enterostatinmentioning

confidence: 99%

Enterostatin‐A Peptide Regulating Fat Intake

Erlanson–Albertsson

York

1997

Obesity Research

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YORK. Enterostatin-a peptide regulating fat intake. Obes Res. 1997;5:360-372. A high fat intake, together with an inability to match lipid oxidation to fat intake, has been found to be correlated with obesity in humans. This review describes our current understanding of enterostatin, a peptide that selectively reduces fat intake. Enterostatin is formed in the intestine by the cleavage of secreted pancreatic procolipase, the remaining colipase serving as an obligatory cofactor for pancreatic lipase during fat digestion. Enterostatin is also produced in the gastric mucosa and the mucosal epithelia of the small intestine. Procolipase gene transcription and enterostatin release into the gastrointestinal lumen are increased by high-fat diets. After feeding, enterostatin appears in the lymph and circulation. Enterostatin will selectively inhibit fat intake during normal feeding and in experimental paradigms that involve dietary choice. Its anorectic effect has been demonstrated in a number of species. Both peripheral and central sites of action have been proposed. The peripheral mechanism involves an afferent vagal signaling pathway to hypothalamic centers. The central responses are mediated through a pathway that includes both serotonergic and opioidergic components. Chronically, enterostatin reduces fat intake, bodyweight, and body fat. This response may involve multiple metabolic effects of enterostatin, which include a reduction of insulin secretion, an increase in sympathetic drive to brown adipose tissue, and the stimulation of adrenal corticosteroid secretion. A possible pathophysiological role is suggested by studies that have linked low enterostatin production andor responsiveness to strains of rat that become obese and prefer dietary fat. Humans with obesity also exhibit a lower secretion of pancreatic procolipase after a test meal, compared with persons of normal weight.

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Opiate blockade inhibits saccharin intake and blocks normal preference acquisition

Cited by 112 publications

References 16 publications

Differential Regulation of the Consummatory, Motivational and Anticipatory Aspects of Feeding Behavior by Dopaminergic and Opioidergic Drugs

Differential Regulation of the Consummatory, Motivational and Anticipatory Aspects of Feeding Behavior by Dopaminergic and Opioidergic Drugs

Reduced alcohol consumption in mice lacking preprodynorphin

Enterostatin‐A Peptide Regulating Fat Intake

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