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

Barbano, M. Flavia; Cador, Martine

doi:10.1038/sj.npp.1300908

Cited by 113 publications

(92 citation statements)

References 67 publications

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“…Our finding that the food-paired context acquired the ability to evoke a conditioned locomotor response is consistent with observations (Bindra, 1968) that environmental stimuli paired with primary reinforcers stimulate locomotor activity, an effect that has been repeatedly confirmed (Jones and Robbins, 1992;Hayward and Low, 2005;Barbano and Cador, 2006). Furthermore, the locomotor activity observed in food-sensitized animals exposed to the food-paired context when food was omitted, was similar in amplitude to their activity measured when food was available.…”

Section: Discussionsupporting

confidence: 90%

Food-Induced Behavioral Sensitization, Its Cross-Sensitization to Cocaine and Morphine, Pharmacological Blockade, and Effect on Food Intake

Merrer

Stephens

2006

J. Neurosci.

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Repeated administration of abused drugs sensitizes their stimulant effects and results in a drug-paired environment eliciting conditioned activity. We tested whether food induces similar effects. Food-deprived male mice were given novel food during 30 min tests in a runway (FR group) that measured locomotor activity. Whereas the activity of this group increased with repeated testing, that of a group exposed to the runways but that received the food in the home cage (FH group), or of a group satiated by prefeeding before testing (SAT group), decreased. When exposed to the runways in the absence of food, the paired group was more active than the other groups (conditioned activity); no activity differences were seen in an alternative, non-food-paired, apparatus. Conditioned activity survived a 3-week period without runway exposure.

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Section: Discussionsupporting

confidence: 90%

Food-Induced Behavioral Sensitization, Its Cross-Sensitization to Cocaine and Morphine, Pharmacological Blockade, and Effect on Food Intake

Merrer

Stephens

2006

J. Neurosci.

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“…The differential actions of nalmefene on chow intake according to diet history support the hypothesis that opioids also participate in learned associative, appetitive processes that underlie food acceptance and selection (Barbano and Cador, 2006;Jarosz et al, 2006;Kas et al, 2004). This conclusion differs from prevailing views that opioid-receptor antagonists simply are anorectic per se (especially for palatable food) or modulate putative 'intrinsic' hedonic properties of foods (Cooper, 2004;de Zwaan and Mitchell, 1992).…”

Section: Discussionmentioning

confidence: 54%

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

131

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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“…For example, motivation or 'wanting' for food is linked with opioid-and dopaminergicmediated signaling within the nucleus accumbens (see reference Berridge et al (2009) for review). Mu-opioid receptor antagonists (eg b-funaltrexamine (BFNA), naloxone) administered either directly into the nucleus accumbens shell (Shin et al, 2010) or peripherally (Wakonigg et al, 2003;Barbano and Cador, 2006) increase the runway time to obtain food. In these studies the increased runway time by opioid receptor blockade either did not differ across trials (Shin et al, 2010) or was enhanced on later trials compared with earlier trials (Wakonigg et al, 2003;Barbano and Cador, 2006).…”

Section: Discussionmentioning

confidence: 99%

“…Mu-opioid receptor antagonists (eg b-funaltrexamine (BFNA), naloxone) administered either directly into the nucleus accumbens shell (Shin et al, 2010) or peripherally (Wakonigg et al, 2003;Barbano and Cador, 2006) increase the runway time to obtain food. In these studies the increased runway time by opioid receptor blockade either did not differ across trials (Shin et al, 2010) or was enhanced on later trials compared with earlier trials (Wakonigg et al, 2003;Barbano and Cador, 2006). This contrasts with the effect of VHPC leptin on runway performance in the present study, which increased the latency to start on early but not later trials relative to vehicle treatment.…”

Section: Discussionmentioning

confidence: 99%

Hippocampal Leptin Signaling Reduces Food Intake and Modulates Food-Related Memory Processing

Kanoski

Hayes

Greenwald

et al. 2011

Neuropsychopharmacol

132

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The increase in obesity prevalence highlights the need for a more comprehensive understanding of the neural systems controlling food intake; one that extends beyond food intake driven by metabolic need and considers that driven by higher-order cognitive factors. The hippocampus, a brain structure involved in learning and memory function, has recently been linked with food intake control. Here we examine whether administration of the adiposity hormone leptin to the dorsal and ventral sub-regions of the hippocampus influences food intake and memory for food. Leptin (0.1 mg) delivered bilaterally to the ventral hippocampus suppressed food intake and body weight measured 24 h after administration; a higher dose (0.4 mg) was needed to suppress intake following dorsal hippocampal delivery. Leptin administration to the ventral but not dorsal hippocampus blocked the expression of a conditioned place preference for food and increased the latency to run for food in an operant runway paradigm. Additionally, ventral but not dorsal hippocampal leptin delivery suppressed memory consolidation for the spatial location of food, whereas hippocampal leptin delivery had no effect on memory consolidation in a non-spatial appetitive response paradigm. Collectively these findings indicate that ventral hippocampal leptin signaling contributes to the inhibition of food-related memories elicited by contextual stimuli. To conclude, the results support a role for hippocampal leptin signaling in the control of food intake and food-related memory processing.

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

Cited by 113 publications

References 67 publications

Food-Induced Behavioral Sensitization, Its Cross-Sensitization to Cocaine and Morphine, Pharmacological Blockade, and Effect on Food Intake

Food-Induced Behavioral Sensitization, Its Cross-Sensitization to Cocaine and Morphine, Pharmacological Blockade, and Effect on Food Intake

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

Hippocampal Leptin Signaling Reduces Food Intake and Modulates Food-Related Memory Processing

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