Food Anticipatory Activity on Circadian Time Scales Is Not Dependent on Central Serotonin: Evidence From Tryptophan Hydroxylase-2 and Serotonin Transporter Knockout Mice

Gallardo, Christian M.; Martin, Camille S.; Steele, Andrew D.

doi:10.3389/fnmol.2020.534238

Cited by 7 publications

(4 citation statements)

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“…When the availability of food is time restricted, the dorsal striatum is proposed to function as a food‐entrained oscillator, resulting in food anticipatory activity with a circadian rhythm that is synced to the food availability time schedule 134 . The role of serotonin signaling in food anticipatory activity is debated: where previous studies have suggested that whole‐brain serotonin signaling suppresses the development of food anticipatory activity, 135,136 a more recent study reported food anticipatory activity to be independent of serotonin signaling 137 . Serotonergic signaling in the dorsal striatum is more strongly related to the regulation of motor behavior, and perturbed serotonergic signaling within this region is associated with several pathological motor conditions 138,139 …”

Section: Functional Organization Of Serotonergic Signaling In Eating Behaviormentioning

confidence: 99%

Serotonin, food intake, and obesity

2021

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Summary The role of serotonin in food intake has been studied for decades. Food intake is mainly regulated by two brain circuitries: (i) the homeostatic circuitry, which matches energy intake to energy expenditure, and (ii) the hedonic circuitry, which is involved in rewarding and motivational aspects of energy consumption. In the homeostatic circuitry, serotonergic signaling contributes to the integration of metabolic signals that convey the body's energy status and facilitates the ability to suppress food intake when homeostatic needs have been met. In the hedonic circuitry, serotonergic signaling may reduce reward‐related, motivational food consumption. In contrast, peripherally acting serotonin promotes energy absorption and storage. Disturbed serotonergic signaling is associated with obesity, emphasizing the importance to understand the role of serotonergic signaling in food intake. However, unraveling the serotonin‐mediated regulation of food intake is complex, as the effects of serotonergic signaling in different brain regions depend on the regional expression of serotonin receptor subtypes and downstream effects via connections to other brain regions. We therefore provide an overview of the effects of serotonergic signaling in brain regions of the homeostatic and hedonic regulatory systems on food intake. Furthermore, we discuss the disturbances in serotonergic signaling in obesity and its potential therapeutic implications.

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Section: Functional Organization Of Serotonergic Signaling In Eating Behaviormentioning

confidence: 99%

Serotonin, food intake, and obesity

2021

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“…Serotonin ablation did not impact the typical day/night fluctuations in mouse activity observed as a response to changes in environmental light. Despite known interactions between serotonin and circadian control systems (regulation of the sleep-wake cycle) and their respective roles in the expression of seasonal mood disorders for instance (Gallardo et al, 2020), this result confirms the role of a larger neurobiological network for the regulation of these homeostatic processes. Moreover, the lack of congenital serotonin did not abolish the expression of any specific behaviour in mice, however it drastically affected their relative frequencies.…”

Section: Discussionmentioning

confidence: 55%

Serotonin drives aggression and social behaviours of laboratory mice in a semi-natural environment

Rivalan,

Alonso,

Mosienko

et al. 2024

Preprint

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Aggression is an adaptive social behaviour crucial for the stability and prosperity of social groups. When uncontrolled, aggression leads to pathological violence that disrupts group structure and individual well-being. The comorbidity of uncontrolled aggression across different psychopathologies makes it a potential endophenotype of mental disorders with the same neurobiological substrates. Serotonin plays a critical role in the regulation of impulsive and aggressive behaviours, and mice lacking brain serotonin, due to the ablation of a rate-limiting enzyme of serotonin synthesis (Tryptophan hydroxylase 2, TPH2), are a potential model of pathological aggression. Home cage monitoring allows for the continuous observation and quantification of social and non-social behaviours in group-housed, freely-moving mice. Using an ethological approach, we investigated the impact of central serotonin ablation on everyday expression of social and non-social behaviours and their correlations in undisturbed, group-living Tph2-deficient and wildtype mice. By training a machine learning algorithm on behavioural time series, allogrooming, struggling at feeder and eating emerged as key behaviours dissociating one genotype from the other. Although Tph2-deficient mice showed characteristics of pathological aggression and decreased communication compared to wildtype animals, they still showed affiliative behaviours to normal levels. Altogether, such distinct and dynamic phenotype of Tph2-deficient mice influenced the group's structure and the dynamic of its hierarchical organization, which emerged later. These aspects were analysed using social network analysis and the Glicko rating methods. This study demonstrates the importance of the ethological approach for understanding the global impact of pathological aggression on different aspects of life, both at the individual and the group level. Home cage monitoring allows the observation of the natural behaviours of the mice in a semi-natural habitat and provides an accurate representation of real-world phenomena and pathological mechanisms. The results of this study provide insights into the neurobiological substrate of pathological aggression and their potential role in complex brain disorders.

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“…Pharmacologically increasing serotonin levels by a selective serotonin reuptake inhibitor, fluvoxamine, suppressed FAA, whereas decreasing serotonin levels by a tryptophan hydroxylase inhibitor enhanced FAA in mice ( Rozenblit-Susan et al, 2016 ). However, FAA was unaffected by time RF in both serotonin transporter and tryptophan hydroxylase-2 KO mice, which indicated that serotonin is not necessary for regulating FAA ( Gallardo et al, 2020 ). Some studies suggested that a neuropeptide knows as orexin or hypocretin may be involved in the regulation of food anticipation behavior.…”

Section: Discussionmentioning

confidence: 99%

Effect of Restricted Feeding on Metabolic Health and Sleep-Wake Rhythms in Aging Mice

Qian

et al. 2021

Front. Neurosci.

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Aging, an irreversible and unavoidable physiological process in all organisms, is often accompanied by obesity, diabetes, cardiovascular diseases, sleep disorders, and fatigue. Thus, older adults are more likely to experience metabolic symptoms and sleep disturbances than are younger adults. Restricted feeding (RF) is a dietary regimen aimed at improving metabolic health and extending longevity, as well as reorganizing sleep-wake cycles. However, the potential of RF to improve metabolic health and sleep quality in older adults who are known to show a tendency toward increased weight gain and decreased sleep is unknown. To elucidate this issue, aged mice were assigned to an RF protocol during the active phase for 2 h per day for 2 weeks. Sleep-wake cycles were recorded during the RF regime in RF group and control mice. At the end of this period, body weight and blood biochemistry profiles, including blood glucose, cholesterol, and enzyme activity, in addition to dopamine concentrations in the brain, were measured in the RF group and age-matched controls. RF for 2 weeks improved the metabolic health of aged mice by reducing their body weights and blood glucose and cholesterol levels. At the beginning of the RF regime, sleep decreased in the dark period but not in the light period. After stable food entrainment was achieved (7 days post-RF commencement), the amount of time spent in wakefulness during the light period dramatically increased for 2 h before food availability, thereby increasing the mean duration of awake episodes and decreasing the number of wakefulness episodes. There was no significant difference in the sleep-wake time during the dark period in the RF group, with similar total amounts of wakefulness and sleep in a 24-h period to those of the controls. During the RF regime, dopamine levels in the midbrain increased in the RF group, pointing to its potential as the mechanism mediating metabolic symptoms and sleep-wake regulation during RF. In conclusion, our study suggested that RF during aging might prohibit or delay the onset of age-related diseases by improving metabolic health, without having a severe deleterious effect on sleep.

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Food Anticipatory Activity on Circadian Time Scales Is Not Dependent on Central Serotonin: Evidence From Tryptophan Hydroxylase-2 and Serotonin Transporter Knockout Mice

Cited by 7 publications

References 50 publications

Serotonin, food intake, and obesity

Serotonin, food intake, and obesity

Serotonin drives aggression and social behaviours of laboratory mice in a semi-natural environment

Effect of Restricted Feeding on Metabolic Health and Sleep-Wake Rhythms in Aging Mice

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