Entrainment by a palatable meal induces food-anticipatory activity and c-Fos expression in reward-related areas of the brain

Mendoza, Jorge; Ángeles-Castellanos, Manuel; Escobar, Carolina

doi:10.1016/j.neuroscience.2005.01.064

Cited by 104 publications

(102 citation statements)

References 46 publications

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“…LAcbSh neurons seem to be exclusively activated after four HFD consumption events, while MAcbSh neurons are similarly activated after one or four HFD consumption events. The Acb activation presumably occurs as a consequence of the VTA dopamine neurons activation, since food rewards trigger phasic Acb dopamine release that, in turn, increases c-Fos (Day et al, 2007;Mendoza et al, 2005;Park and Carr, 1998). Current results suggest that consummatory rather than anticipatory aspects of feeding are associated with the activation of the mesolimbic pathway.…”

Section: Discussionmentioning

confidence: 65%

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: Discussionmentioning

confidence: 65%

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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“…Using circadian time as a cue predicting food availability as it occurs in scheduled feeding paradigms, ghrelin- and GHSRknockout animals exhibited blunted feeding responses, even though they had no impairment in normal feeding or rebound feeding after an acute 24-hour fast. In light of the facts that repeated fasting is associated with increased activity both in cells in hypothalamic centers regulating energy balance and in cells in target regions of the VTA and that ghrelin stimulates DA release in these same regions, it is possible that the lack of ghrelin or GHSRs leads to impairments in mechanisms related to food anticipation (29,30,44). On the other hand, rebound feeding after an acute fast was not altered in adult GHSR-knockout mice, but was decreased in normal adult mice infused with a GHSR antagonist into the VTA.…”

Section: Discussionmentioning

confidence: 99%

“…There is a substantial amount of evidence supporting the notion that cues predicting access to rewards such as food are as effective in activating the mesolimbic reward system as the rewards themselves (15,16,28). Temporal cues that predict food availability are of particular interest because they seem to activate reward circuits and to generate behavioral food-anticipatory responses like increased locomotor activity that could be associated with increased activity of the mesolimbic dopaminergic system (29,30). Because of this, and to further examine whether ghrelin has any physiologic effect on food intake, we analyzed ghrelin-knockout and GHSR-knockout animals on a restricted feeding schedule ( Figure 5, G and H).…”

Section: Peripheral Ghrelin-induced Feeding Responses In Rats Are Attmentioning

confidence: 99%

Ghrelin modulates the activity and synaptic input organization of midbrain dopamine neurons while promoting appetite

et al. 2006

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The gut hormone ghrelin targets the brain to promote food intake and adiposity. The ghrelin receptor growth hormone secretagogue 1 receptor (GHSR) is present in hypothalamic centers controlling energy metabolism as well as in the ventral tegmental area (VTA), a region important for motivational aspects of multiple behaviors, including feeding. Here we show that in mice and rats, ghrelin bound to neurons of the VTA, where it triggered increased dopamine neuronal activity, synapse formation, and dopamine turnover in the nucleus accumbens in a GHSR-dependent manner. Direct VTA administration of ghrelin also triggered feeding, while intra-VTA delivery of a selective GHSR antagonist blocked the orexigenic effect of circulating ghrelin and blunted rebound feeding following fasting. In addition, ghrelin-and GHSR-deficient mice showed attenuated feeding responses to restricted feeding schedules. Taken together, these data suggest that the mesolimbic reward circuitry is targeted by peripheral ghrelin to influence physiological mechanisms related to feeding.

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“…34 As the anticipation of daily feeding in food-restricted rats can reduce behavioral motivation in instrumental tasks and shift circadian rhythms, the rats were fed no less than 2 hours after the last rats finished behavioral testing (~8 PM). It has been shown that the body temperature and behavioral activity of food-restricted rats increases approximately 1 hour before the daily consumption of rat chow 35,36 and before regular feedings of midday sucrose solution (~20 kcal) presented 8 hours before daily feeding. 37 Although the current behavioral task provided smaller quantities of sucrose (~11 kcal) at less regular intervals (5 days weekly), it is possible that the rats' waking schedule was similarly shifted before testing and that they were sleep deprived for as little as 3, 6, and 9 hours from their actual sleeping times.…”

Section: Experimental Designmentioning

confidence: 99%

Sleep Deprivation in Rats Produces Attentional Impairments on a 5-Choice Serial Reaction Time Task

Córdova

Said

McCarley

et al. 2006

Sleep

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Study Objectives-To develop a rodent model of the attentional dysfunction caused by sleep loss.Design-The attentional performance of rats was assessed after 4, 7, and 10 hours of total sleep deprivation on a 5-choice serial reaction time task, in which rats detect and respond to brief visual stimuli.Setting-The rats were housed, sleep deprived, and behaviorally tested in a controlled laboratory setting.Participants-Ten male Long-Evans rats were used in the study.Interventions-Rats were trained to criteria and subsequently tested in daily sessions of 100 trials at approximately 4:00 PM (lights on 8:00 AM-8:00 PM). Attentional performance was measured after 4, 7, 10 hours of total sleep deprivation induced by gentle handling.Results-Sleep deprivation produced a monotonic increase in response latencies across the 4-hour, 7-hour, and 10-hour deprivations. Sleep deprivation also led to increased omission errors, but the overall number of perseverative and premature responses was unchanged. Subgroups of rats were differentially affected in the number of omission errors and perseverative responses.Conclusions-The effects of sleep deprivation on rats are compatible with a range of human findings on the effects of sleepiness on selective attention, psychomotor vigilance, and behavioral control. Rats also exhibited differential susceptibility to the effects of sleep deprivation, consistent with 'trait-like' susceptibility that has been found in humans. These findings indicate the feasibility of using the 5-choice serial reaction time task as an animal model for investigating the direct links between homeostatic sleep mechanisms and resulting attentional impairments within a single animal subject.

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Entrainment by a palatable meal induces food-anticipatory activity and c-Fos expression in reward-related areas of the brain

Cited by 104 publications

References 46 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

Ghrelin modulates the activity and synaptic input organization of midbrain dopamine neurons while promoting appetite

Sleep Deprivation in Rats Produces Attentional Impairments on a 5-Choice Serial Reaction Time Task

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