The neuropharmacology of relapse to food seeking: Methodology, main findings, and comparison with relapse to drug seeking

Nair, Sunila G; Adams‐Deutsch, Tristan; Epstein, David H.; Shaham, Yavin

doi:10.1016/j.pneurobio.2009.05.003

Cited by 103 publications

(135 citation statements)

References 342 publications

(470 reference statements)

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“…However, no effect on delay discounting, a measure of impulsive choice, was observed. At doses that reduced impulsive-like behaviour, both drugs also inhibited the cue-induced reinstatement of food-seeking behaviours, a proposed measure of dietary relapse (Nair et al 2009;Calu et al 2014;Guy et al 2011). These effects of lorcaserin and CP-809101 were apparent at doses lower than those required to reduce food intake in response to energy deficit.…”

Section: Discussionmentioning

confidence: 94%

“…Together these three tasks, each with a human analogue, are widely used to study impulsivity across species and offer opportunities for translational research (Dalley et al 2011;Winstanley 2011). Given the association between impulsive behaviour and relapse of drug seeking, we then studied the effects of both lorcaserin and CP-809101 on a test of cue-induced reinstatement of food-seeking behaviour, a proposed model of dietary relapse (Nair et al 2009;Calu et al 2014;Pratt and Ford 2013). Finally, both 5-HT 2C receptor agonists were also studied at equivalent doses for effect against feeding induced by hunger and energy demand.…”

Section: Introductionmentioning

confidence: 99%

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Lorcaserin and CP-809101 reduce motor impulsivity and reinstatement of food seeking behavior in male rats: Implications for understanding the anti-obesity property of 5-HT2C receptor agonists

Higgins

Silenieks²,

Altherr

et al. 2016

Psychopharmacology

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These results suggest that in addition to previously reported effects on satiety and reward, altered impulse control may represent a contributory factor to the anti-obesity property of 5-HT2C receptor agonists. Lorcaserin may promote weight loss by improving adherence to dietary regimens in individuals otherwise prone to relapse and may be beneficial in cases where obesity is associated with eating disorders tied to impulsive traits, such as binge eating disorder.

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Section: Discussionmentioning

confidence: 94%

Section: Introductionmentioning

confidence: 99%

Lorcaserin and CP-809101 reduce motor impulsivity and reinstatement of food seeking behavior in male rats: Implications for understanding the anti-obesity property of 5-HT2C receptor agonists

Higgins

Silenieks²,

Altherr

et al. 2016

Psychopharmacology

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“…Priming effects, whereby initial exposure to foodrelated cues or food consumption influences food intake, have been observed in humans and rodents (2,3,18,19 24-h SHF had increased distance traveled and entries into the food zone 2 d after, but not immediately after, the "priming" experience, unless VTA insulin receptors were blocked. This effect could be due to increased interest in SHF or to an increase in risk-taking associated with a potential withdrawal from the food (21).…”

Section: Discussionmentioning

confidence: 99%

Consumption of palatable food primes food approach behavior by rapidly increasing synaptic density in the VTA

Liu

Globa

Mills

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

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In an environment with easy access to highly palatable and energydense food, food-related cues drive food-seeking regardless of satiety, an effect that can lead to obesity. The ventral tegmental area (VTA) and its mesolimbic projections are critical structures involved in the learning of environmental cues used to predict motivationally relevant outcomes. Priming effects of food-related advertising and consumption of palatable food can drive food intake. However, the mechanism by which this effect occurs, and whether these priming effects last days after consumption, is unknown. Here, we demonstrate that short-term consumption of palatable food can prime future food approach behaviors and food intake. This effect is mediated by the strengthening of excitatory synaptic transmission onto dopamine neurons that is initially offset by a transient increase in endocannabinoid tone, but lasts days after an initial 24-h exposure to sweetened high-fat food (SHF). This enhanced synaptic strength is mediated by a long-lasting increase in excitatory synaptic density onto VTA dopamine neurons. Administration of insulin into the VTA, which suppresses excitatory synaptic transmission onto dopamine neurons, can abolish food approach behaviors and food intake observed days after 24-h access to SHF. These results suggest that even a short-term exposure to palatable foods can drive future feeding behavior by "rewiring" mesolimbic dopamine neurons.palatable food | synaptic density | VTA | dopamine | excitatory synaptic transmission P riming effects of food-related advertising (1) and consumption of palatable food (2, 3) can drive sated consumption of food. Overconsumption of food relative to need is an important factor in the development of obesity (4). The priming effects of palatable food on food intake are likely a considerable factor in the obesity epidemic. However, the mechanism by which food-priming effects occur is unknown. The ventral tegmental area (VTA) and its mesolimbic projections are critical for learning about environmental cues used to predict motivationally relevant outcomes (5). Indeed, food-related cues activate the dopaminergic circuit to reinforce food intake (6, 7). VTA dopamine neurons can increase or decrease their synaptic efficacy to modulate their consequent dopaminergic output (8, 9). The strength of excitatory synaptic input onto VTA dopamine neurons plays a central role in rewardrelated behavior with potentiation of synapses formed onto VTA neurons, facilitating the transformation of neutral environmental stimuli into salient reward predictive cues (8). Conversely, depression of excitatory synaptic transmission would likely reduce the intrinsic firing rate and excitability of dopamine neurons, as has been demonstrated for other neurons (10), and would likely reduces the salience of reward predicting cues.The motivation to eat is regulated by a variety of intrinsic and extrinsic factors. Metabolic signals, including neuronal or circulating peptides released in response to internal states such as hunger ...

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“…Food seeking can be reinstated by non-contingent presentation of food, or response-contingent presentation of food-associated conditioned stimuli. Although reinstatement to food or drug seeking does not equate to addiction-like behavior, it has been shown that animals that had lost control over cocaine intake (as assessed using the 3-criteria model), were more prone to reinstatement of cocaine seeking [78], and the neural substrates of reinstatement of food and drug seeking overlap to some degree [133]. …”

Section: Models For Aspects Of Food Addiction-like Behavior and Neuromentioning

confidence: 99%

Towards an Animal Model of Food Addiction

Jong¹,

Vanderschuren²,

Adan³

2012

Obes Facts

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The dramatically increasing prevalence of obesity, associated with potentially life-threatening health problems, including cardiovascular diseases and type II diabetes, poses an enormous public health problem. It has been proposed that the obesity epidemic can be explained by the concept of ‘food addiction’. In this review we focus on possible similarities between binge eating disorder (BED), which is highly prevalent in the obese population, and drug addiction. Indeed, both behavioral and neural similarities between addiction and BED have been demonstrated. Behavioral similarities are reflected in the overlap in DSM-IV criteria for drug addiction with the (suggested) criteria for BED and by food addiction-like behavior in animals after prolonged intermittent access to palatable food. Neural similarities include the overlap in brain regions involved in food and drug craving. Decreased dopamine D2 receptor availability in the striatum has been found in animal models of binge eating, after cocaine self-administration in animals as well as in drug addiction and obesity in humans. To further explore the neurobiological basis of food addiction, it is essential to have an animal model to test the addictive potential of palatable food. A recently developed animal model for drug addiction involves three behavioral characteristics that are based on the DSM-IV criteria: i) extremely high motivation to obtain the drug, ii) difficulty in limiting drug seeking even in periods of explicit non-availability, iii) continuation of drug-seeking despite negative consequences. Indeed, it has been shown that a subgroup of rats, after prolonged cocaine self-administration, scores positive on these three criteria. If food possesses addictive properties, then food-addicted rats should also meet these criteria while searching for and consuming food. In this review we discuss evidence from literature regarding food addiction-like behavior. We also suggest future experiments that could further contribute to our understanding of behavioral and neural commonalities and differences between obesity and drug addiction.

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The neuropharmacology of relapse to food seeking: Methodology, main findings, and comparison with relapse to drug seeking

Cited by 103 publications

References 342 publications

Lorcaserin and CP-809101 reduce motor impulsivity and reinstatement of food seeking behavior in male rats: Implications for understanding the anti-obesity property of 5-HT2C receptor agonists

Lorcaserin and CP-809101 reduce motor impulsivity and reinstatement of food seeking behavior in male rats: Implications for understanding the anti-obesity property of 5-HT2C receptor agonists

Consumption of palatable food primes food approach behavior by rapidly increasing synaptic density in the VTA

Towards an Animal Model of Food Addiction

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