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The dilemmas of the gourmet fly: the molecular and neuronal mechanisms of feeding and nutrient decision making in Drosophila.

Itskov PM, Ribeiro C - Front Neurosci (2013)

Bottom Line: To survive and successfully reproduce animals need to maintain a balanced intake of nutrients and energy.This review discusses methodologies developed in order to study insect feeding, the effects of neuropeptides and neuromodulators on feeding behavior, behavioral evidence supporting the existence of internal energy sensors, neuronal and molecular mechanisms controlling protein intake, and finally the regulation of feeding by circadian rhythms and sleep.From the discussed data a conceptual framework starts to emerge which aims to explain the molecular and neuronal processes maintaining the stability of the internal milieu.

View Article: PubMed Central - PubMed

Affiliation: Behaviour and Metabolism Laboratory, Champalimaud Neuroscience Programme, Champalimaud Centre for the Unknown Lisbon, Portugal.

ABSTRACT
To survive and successfully reproduce animals need to maintain a balanced intake of nutrients and energy. The nervous system of insects has evolved multiple mechanisms to regulate feeding behavior. When animals are faced with the choice to feed, several decisions must be made: whether or not to eat, how much to eat, what to eat, and when to eat. Using Drosophila melanogaster substantial progress has been achieved in understanding the neuronal and molecular mechanisms controlling feeding decisions. These feeding decisions are implemented in the nervous system on multiple levels, from alterations in the sensitivity of peripheral sensory organs to the modulation of memory systems. This review discusses methodologies developed in order to study insect feeding, the effects of neuropeptides and neuromodulators on feeding behavior, behavioral evidence supporting the existence of internal energy sensors, neuronal and molecular mechanisms controlling protein intake, and finally the regulation of feeding by circadian rhythms and sleep. From the discussed data a conceptual framework starts to emerge which aims to explain the molecular and neuronal processes maintaining the stability of the internal milieu.

No MeSH data available.


Related in: MedlinePlus

Regulation of gustatory processing and feeding behavior by starvation. (A) In satiated animals, leucokinin is released in response to the filling of the crop and gut occurring after feeding. Leucokinin affects unknown populations of neurons in the nervous system via leucokinin receptors resulting in the termination of feeding. In the same animals TH-VUM dopaminergic neurons are less active and Gr5a expressing GRNs produce a weak response to “sweet” compounds. (B) In starved animals, the spiking activity of TH-VUM neurons is increased leading to dopamine release on the Gr5a expressing GRNs. In these GRNs dopamine binds to the DopEcR receptor causing increase in the calcium response to “sweet” compounds. As the crop and gut are empty leucokinin release is inhibited and feeding termination does not occur.
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Figure 2: Regulation of gustatory processing and feeding behavior by starvation. (A) In satiated animals, leucokinin is released in response to the filling of the crop and gut occurring after feeding. Leucokinin affects unknown populations of neurons in the nervous system via leucokinin receptors resulting in the termination of feeding. In the same animals TH-VUM dopaminergic neurons are less active and Gr5a expressing GRNs produce a weak response to “sweet” compounds. (B) In starved animals, the spiking activity of TH-VUM neurons is increased leading to dopamine release on the Gr5a expressing GRNs. In these GRNs dopamine binds to the DopEcR receptor causing increase in the calcium response to “sweet” compounds. As the crop and gut are empty leucokinin release is inhibited and feeding termination does not occur.

Mentions: Another neuropeptide, leucokinin, which is a potential homolog of mammalian Tachykinin, may signal the amount of food in the foregut and thus controls the termination of the meal (Figure 2). This is apparent from the behavioral phenotypes of both leucokinin and leucokinin receptor mutants: the mutant animals increase the amount of food they consume per meal and, as a compensation, increase the inter-meal interval, keeping the caloric intake constant (Al-Anzi et al., 2010). The same behavioral phenotype can be observed in animals with ablated leucokinin expressing neurons. Neuronal leucokinin is responsible for this phenotype since the phenotype can be rescued by the pan-neuronal expression of either the peptide or its receptor. Furthermore, the effect of leucokinin appears to be independent of hugin and npf neurons since their ablation does not affect meal size (Al-Anzi et al., 2010). In short, leucokinin appears to mediate the decision to stop feeding.


The dilemmas of the gourmet fly: the molecular and neuronal mechanisms of feeding and nutrient decision making in Drosophila.

Itskov PM, Ribeiro C - Front Neurosci (2013)

Regulation of gustatory processing and feeding behavior by starvation. (A) In satiated animals, leucokinin is released in response to the filling of the crop and gut occurring after feeding. Leucokinin affects unknown populations of neurons in the nervous system via leucokinin receptors resulting in the termination of feeding. In the same animals TH-VUM dopaminergic neurons are less active and Gr5a expressing GRNs produce a weak response to “sweet” compounds. (B) In starved animals, the spiking activity of TH-VUM neurons is increased leading to dopamine release on the Gr5a expressing GRNs. In these GRNs dopamine binds to the DopEcR receptor causing increase in the calcium response to “sweet” compounds. As the crop and gut are empty leucokinin release is inhibited and feeding termination does not occur.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3569668&req=5

Figure 2: Regulation of gustatory processing and feeding behavior by starvation. (A) In satiated animals, leucokinin is released in response to the filling of the crop and gut occurring after feeding. Leucokinin affects unknown populations of neurons in the nervous system via leucokinin receptors resulting in the termination of feeding. In the same animals TH-VUM dopaminergic neurons are less active and Gr5a expressing GRNs produce a weak response to “sweet” compounds. (B) In starved animals, the spiking activity of TH-VUM neurons is increased leading to dopamine release on the Gr5a expressing GRNs. In these GRNs dopamine binds to the DopEcR receptor causing increase in the calcium response to “sweet” compounds. As the crop and gut are empty leucokinin release is inhibited and feeding termination does not occur.
Mentions: Another neuropeptide, leucokinin, which is a potential homolog of mammalian Tachykinin, may signal the amount of food in the foregut and thus controls the termination of the meal (Figure 2). This is apparent from the behavioral phenotypes of both leucokinin and leucokinin receptor mutants: the mutant animals increase the amount of food they consume per meal and, as a compensation, increase the inter-meal interval, keeping the caloric intake constant (Al-Anzi et al., 2010). The same behavioral phenotype can be observed in animals with ablated leucokinin expressing neurons. Neuronal leucokinin is responsible for this phenotype since the phenotype can be rescued by the pan-neuronal expression of either the peptide or its receptor. Furthermore, the effect of leucokinin appears to be independent of hugin and npf neurons since their ablation does not affect meal size (Al-Anzi et al., 2010). In short, leucokinin appears to mediate the decision to stop feeding.

Bottom Line: To survive and successfully reproduce animals need to maintain a balanced intake of nutrients and energy.This review discusses methodologies developed in order to study insect feeding, the effects of neuropeptides and neuromodulators on feeding behavior, behavioral evidence supporting the existence of internal energy sensors, neuronal and molecular mechanisms controlling protein intake, and finally the regulation of feeding by circadian rhythms and sleep.From the discussed data a conceptual framework starts to emerge which aims to explain the molecular and neuronal processes maintaining the stability of the internal milieu.

View Article: PubMed Central - PubMed

Affiliation: Behaviour and Metabolism Laboratory, Champalimaud Neuroscience Programme, Champalimaud Centre for the Unknown Lisbon, Portugal.

ABSTRACT
To survive and successfully reproduce animals need to maintain a balanced intake of nutrients and energy. The nervous system of insects has evolved multiple mechanisms to regulate feeding behavior. When animals are faced with the choice to feed, several decisions must be made: whether or not to eat, how much to eat, what to eat, and when to eat. Using Drosophila melanogaster substantial progress has been achieved in understanding the neuronal and molecular mechanisms controlling feeding decisions. These feeding decisions are implemented in the nervous system on multiple levels, from alterations in the sensitivity of peripheral sensory organs to the modulation of memory systems. This review discusses methodologies developed in order to study insect feeding, the effects of neuropeptides and neuromodulators on feeding behavior, behavioral evidence supporting the existence of internal energy sensors, neuronal and molecular mechanisms controlling protein intake, and finally the regulation of feeding by circadian rhythms and sleep. From the discussed data a conceptual framework starts to emerge which aims to explain the molecular and neuronal processes maintaining the stability of the internal milieu.

No MeSH data available.


Related in: MedlinePlus