Activation of mesolimbic dopamine neurons during novel and daily limited access to palatable food is blocked by the opioid antagonist LY255582

Sahr, Allison E.; Sindelar, Dana K.; Alexander-Chacko, Jesline; Eastwood, Brian J.; Mitch, Charles H.; Statnick, Michael A.

doi:10.1152/ajpregu.00390.2007

Cited by 42 publications

(32 citation statements)

References 59 publications

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“…Current results suggest that consummatory rather than anticipatory aspects of feeding are associated with the activation of the mesolimbic pathway. This possibility agrees with previous microdialysis studies showing that Acb dopamine release mainly occurs during the consummatory phase of feeding and not during the anticipatory phase (Sahr et al, 2008;Wilson et al, 1995). Notably, an activation of the MAcbSh neurons was detected in anticipation to the fourth HFD consumption event, similarly as found for the IF dopamine neurons.…”

Section: Discussionsupporting

confidence: 92%

Escalation in high fat intake in a binge eating model differentially engages dopamine neurons of the ventral tegmental area and requires ghrelin signaling

Valdivia¹,

Cornejo²,

Reynaldo³

et al. 2015

Psychoneuroendocrinology

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Please cite this article in press as: Valdivia, S., et al., Escalation in high fat intake in a binge eating model differentially engages dopamine neurons of the ventral tegmental area and requires ghrelin signaling. Psychoneuroendocrinology (2015) and time-limited exposed to a high-fat diet (HFD) display robust binge eating events that gradually escalate over the initial accesses. Intake escalation is proposed to be part of the transition from a controlled to a compulsive or loss of control behavior. Here, we used a combination of behavioral and neuroanatomical studies in mice daily and time-limited exposed to HFD to determine the neuronal brain targets that are activated -as indicated by the marker of cellular activation c-Fos -under these circumstances. Also, we used pharmacologically or genetically manipulated mice to study the role of orexin or ghrelin signaling, respectively, in the modulation of this behavior. We found that four daily and time-limited accesses to HFD induce: (i) a robust hyperphagia with an escalating profile, (ii) an activation of different sub-populations of the ventral tegmental area dopamine neurons and accumbens neurons that is, in general, more pronounced than the activation observed after a single HFD consumption event, and (iii) an activation of the hypothalamic orexin neurons, although orexin signaling blockage fails to affect escalation of HFD intake. In addition, we found that ghrelin receptor-deficient mice fail to both escalate the HFD consumption over the successive days of exposure and fully induce activation of the mesolimbic pathway in response to HFD consumption. Current data suggest that the escalation in high fat intake during repeated accesses differentially engages dopamine neurons of the ventral tegmental area and requires ghrelin signaling.

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Section: Discussionsupporting

confidence: 92%

Escalation in high fat intake in a binge eating model differentially engages dopamine neurons of the ventral tegmental area and requires ghrelin signaling

Valdivia¹,

Cornejo²,

Reynaldo³

et al. 2015

Psychoneuroendocrinology

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“…The first report showing that blockade of opioid receptors decreases food intake used naloxone, a general opioid receptor antagonist [5]. Since then, numerous studies have established that both systemic and intracerebroventricular administration of general opioid receptor antagonists reduces food intake and body weight in rodent models, including genetically obese Zucker and diet-induced obese rats [6,7,8,9,10]. Accordingly, agonists of the opioid receptors increase food intake [11].…”

Section: Opioid Receptors and Feeding Behavior: Homeostatic And Hedonmentioning

confidence: 99%

“…Similarly, another report found that rats fed on high-fat diet receiving a chronic oral treatment with LY255582 for 14 days reduced body fat by decreasing food intake and stimulating lipid utilization [9]. Furthermore, LY255582 also inhibited the consumption of a highly palatable diet after a 4-day treatment and blocked the activation of mesolimbic dopamine neurons in the nucleus accumbens induced by high palatable diet [10]. Thus, LY255582 appears to be a potent and long-acting anorectic drug.…”

Section: Opioid Receptors and Feeding Behavior: Homeostatic And Hedonmentioning

confidence: 99%

The Opioid System and Food Intake: Homeostatic and Hedonic Mechanisms

Nogueiras¹,

Romero‐Picó²,

Vázquez³

et al. 2012

Obes Facts

121

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Opioids are important in reward processes leading to addictive behavior such as self-administration of opioids and other drugs of abuse including nicotine and alcohol. Opioids are also involved in a broadly distributed neural network that regulates eating behavior, affecting both homeostatic and hedonic mechanisms. In this sense, opioids are particularly implicated in the modulation of highly palatable foods, and opioid antagonists attenuate both addictive drug taking and appetite for palatable food. Thus, craving for palatable food could be considered as a form of opioid-related addiction. There are three main families of opioid receptors (µ, ĸ, and δ) of which µ-receptors are most strongly implicated in reward. Administration of selective µ-agonists into the NAcc of rodents induces feeding even in satiated animals, while administration of µ-antagonists reduces food intake. Pharmacological studies also suggest a role for ĸ- and δ-opioid receptors. Preliminary data from transgenic knockout models suggest that mice lacking some of these receptors are resistant to high-fat diet-induced obesity.

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“…The reason for this is that these foods have the ability to activate the central neural circuits involved in the regulation of motivation and reward (the mesolimbic reward system) in a manner analogous to alcohol and drugs of abuse (20,21). Studies in both humans and animals have shown that the intake of fat and sugar produces acute increases in the synthesis and secretion of opioids and dopamine within the central reward system (22)(23)(24)(25)(26)(27). The similarity between the acute effects of palatable foods and those of well-characterized drugs of abuse has led to the concept that overexposure to palatable foods may also result in long-term alterations to reward pathway sensitivity.…”

Section: High-fat/high-sugar Junk Foods and The Mesolimbic Reward Systemmentioning

confidence: 99%

The early origins of food preferences: targeting the critical windows of development

2015

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The nutritional environment to which an individual is exposed during the perinatal period plays a crucial role in determining his or her future metabolic health outcomes. Studies in rodent models have demonstrated that excess maternal intake of high-fat and/or high-sugar "junk foods" during pregnancy and lactation can alter the development of the central reward pathway, particularly the opioid and dopamine systems, and program an increased preference for junk foods in the offspring. More recently, there have been attempts to define the critical windows of development during which the opioid and dopamine systems within the reward pathway are most susceptible to alteration and to determine whether it is possible to reverse these effects through nutritional interventions applied later in development. This review discusses the progress made to date in these areas, highlights the apparent importance of sex in determining these effects, and considers the potential implications of the findings from rodent models in the human context.-Gugusheff, J. R., Ong, Z. Y., Muhlhausler, B. S. The early origins of food preferences: targeting the critical windows of development. FASEB J. 29, 365-373 (2015). www.fasebj.org Key Words: programming • high-fat diet • reward BOTH HUMAN AND ANIMAL studies have provided compelling evidence that the nutritional environment an individual experiences before birth and/or in early infancy is a key determinant of his/her subsequent metabolic health outcomes. In particular, individuals who are exposed to maternal overnutrition during the perinatal period (i.e., before birth and while breastfeeding/early infancy) have a greater propensity toward excess food intake and weight gain in childhood and adult life (1-6). More recently, animal studies have demonstrated that in addition to predisposing individuals to consume more energy overall, perinatal exposure to high-fat and/or high-sugar diets also increases the preference for palatable "junk foods" in the offspring (7,8).Over the past few years, studies from our group and others have provided novel insights into the biologic mechanisms that underlie the developmental programming of food preferences. These studies have strongly implicated altered development of the central mesolimbic reward system (opioid and dopamine pathways) as a potential mechanism by demonstrating that prenatal fat/ sugar exposure can alter gene expression of key components of this pathway and the way in which it functions. To date, the majority of studies on the mesolimbic reward pathway have focused on the consequences of being exposed to high-fat and/or high-sugar diets during the entire perinatal period. However, given that the development of central reward systems begins before birth and extends into the fourth week of postnatal life in the rodent (9-11), there has been growing interest in defining whether there are "critical windows" of reward pathway development during which exposure to a maternal junk food diet is most detrimental. A critical window for the purpo...

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Activation of mesolimbic dopamine neurons during novel and daily limited access to palatable food is blocked by the opioid antagonist LY255582

Cited by 42 publications

References 59 publications

Escalation in high fat intake in a binge eating model differentially engages dopamine neurons of the ventral tegmental area and requires ghrelin signaling

Escalation in high fat intake in a binge eating model differentially engages dopamine neurons of the ventral tegmental area and requires ghrelin signaling

The Opioid System and Food Intake: Homeostatic and Hedonic Mechanisms

The early origins of food preferences: targeting the critical windows of development

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