Reduced anticipatory locomotor responses to scheduled meals in ghrelin receptor deficient mice

Blum, Ian D.; Patterson, Zachary R.; Khazall, Rim; Lamont, Elaine Waddington; Sleeman, Mark W.; Horváth, Tamas L.; Abizaid, Alfonso

doi:10.1016/j.neuroscience.2009.08.009

Cited by 166 publications

(196 citation statements)

References 38 publications

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“…Interestingly, GHSR-deficient mice also exhibit diminished behavioral activation and reinforcement responses to cocaine and nicotine (Abizaid et al, 2011;Jerlhag and Engel, 2011), and it has been proposed that ghrelin signaling could induce a form of central sensitization in which animals are more reactive to rewarding stimuli (Wellman et al, 2013). Indeed, it has been shown that GHSR-deficient mice display a reduced anticipatory locomotor response to scheduled meals (Blum et al, 2009). To our knowledge, current results are the first report of the requirement of the ghrelin signaling for HFD escalation in rodents.…”

Section: Discussionmentioning

confidence: 99%

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: 99%

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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“…Animals with limited access to food learn to anticipate food availability by increasing locomotion (food anticipatory activity, FAA) and optimize their consummatory behavior during that period. Ghrelin signaling is critical for FAA and consumption (Blum et al, 2009;Verhagen et al, 2011). When assessed on chow diet, we found that total locomotor activity by AgRP-ablated mice was initially decreased relative to control mice but activity recovered by day 5; when the mice were on HFHS diet, the AgRP-ablated group recovered normal locomotion faster ( Figure 7A).…”

Section: Agrp-ablated Mice Display Impaired Feeding But Abnormal Antimentioning

confidence: 93%

Palatability Can Drive Feeding Independent of AgRP Neurons

Denis¹,

Joly‐Amado²,

Webber³

et al. 2017

Cell Metabolism

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“…There is no doubt that FAA stems from activity within the brain, although the initiation of this activity may arise from peripheral oscillating or stimulating processes (38)(39)(40). All in all, the appearance of c-Fos or PERIOD immunoreactivity in many brain areas after food restriction and the failure to prevent FAA by lesioning different brain areas (13) suggests that the organization of the oscillatory nature of FAA should be within a system of interacting brain structures.…”

Section: Faa Is Lost After Lesion Of the Dmh But Reappears After Amentioning

confidence: 99%

Interaction between hypothalamic dorsomedial nucleus and the suprachiasmatic nucleus determines intensity of food anticipatory behavior

Acosta-Galvan

Vliet

et al. 2011

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

158

131

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Food anticipatory behavior (FAA) is induced by limiting access to food for a few hours daily. Animals anticipate this scheduled meal event even without the suprachiasmatic nucleus (SCN), the biological clock. Consequently, a food-entrained oscillator has been proposed to be responsible for meal time estimation. Recent studies suggested the dorsomedial hypothalamus (DMH) as the site for this food-entrained oscillator, which has led to considerable controversy in the literature. Herein we demonstrate by means of c-Fos immunohistochemistry that the neuronal activity of the suprachiasmatic nucleus (SCN), which signals the rest phase in nocturnal animals, is reduced when animals anticipate the scheduled food and, simultaneously, neuronal activity within the DMH increases. Using retrograde tracing and confocal analysis, we show that inhibition of SCN neuronal activity is the consequence of activation of GABA-containing neurons in the DMH that project to the SCN. Next, we show that DMH lesions result in a loss or diminution of FAA, simultaneous with increased activity in the SCN. A subsequent lesion of the SCN restored FAA. We conclude that in intact animals, FAA may only occur when the DMH inhibits the activity of the SCN, thus permitting locomotor activity. As a result, FAA originates from a neuronal network comprising an interaction between the DMH and SCN. Moreover, this study shows that the DMH-SCN interaction may serve as an intrahypothalamic system to gate activity instead of rest overriding circadian predetermined temporal patterns. P hysiology and behavior of all mammals is organized in an alternating pattern of rest and activity cycles, whereby the endogenous and light-induced daily neuronal activity of the suprachiasmatic nucleus (SCN) signals rest in nocturnal rodents and activity in diurnal primates, such as humans (1, 2). Restricting food access to a short and predictable episode during the rest phase changes this behavioral pattern, such that an animal becomes active and for up to several hours anticipates the upcoming feeding event. This food anticipatory activity (FAA) is even exhibited without the known circadian oscillator, the SCN (3), and thus may rely on a different circadian pacemaker.In search of the location of this so-called "food entrained oscillator" (FEO), two recent studies have claimed that its position is within the dorsomedial nucleus of the hypothalamus (DMH) (4, 5). The designation of the DMH as master clock for food entrainment is, however, controversial because some groups reported unimpaired FAA despite large lesions of the DMH (6, 7); others have shown that lesions of the DMH disturb and diminish the intensity of FAA (6). The possible participation of other brain structures in FAA is evident from studies that demonstrate modulation of neuronal activity and induction of clock-gene rhythmicity in hypothalamic and limbic structures by feeding schedules (8-11). Thus, it has been suggested that FAA depends on a multioscillatory system comprised of a complex and redundant neuronal netwo...

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Reduced anticipatory locomotor responses to scheduled meals in ghrelin receptor deficient mice

Cited by 166 publications

References 38 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

Palatability Can Drive Feeding Independent of AgRP Neurons

Interaction between hypothalamic dorsomedial nucleus and the suprachiasmatic nucleus determines intensity of food anticipatory behavior

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