Hückesfeld, Sebastian: The Control of Food Intake and Bitter Taste Information Processing in the Drosophila Larval Brain. - Bonn, 2016. - Dissertation, Rheinische Friedrich-Wilhelms-Universität Bonn.
Online-Ausgabe in bonndoc: https://nbn-resolving.org/urn:nbn:de:hbz:5n-45494
@phdthesis{handle:20.500.11811/6928,
urn: https://nbn-resolving.org/urn:nbn:de:hbz:5n-45494,
author = {{Sebastian Hückesfeld}},
title = {The Control of Food Intake and Bitter Taste Information Processing in the Drosophila Larval Brain},
school = {Rheinische Friedrich-Wilhelms-Universität Bonn},
year = 2016,
month = dec,

note = {The regulation of feeding behavior by central neural circuits is crucial for every organism to survive. Hierarchical organized motor systems are responsible for the execution of appropriate feeding movements and can be subdivided into higher brain centers modulating the activity of central pattern generators (CPGs), which in turn control the activity of motor neurons. Motor neurons innervate muscles whose contractions lead to the final behavioral outcome. Focus of this thesis was the deconstruction of feeding regulatory elements like motor neurons innervating the muscles specific for the Drosophila larval feeding cycle and neural populations modulating their activity. Emphasis relied on the functional relevance for the Hugin neuropeptide concerning feeding behavior and taste processing.
We show that motor neurons comprising the larval feeding movements are located in the subesophageal zone (SEZ) of the larval central nervous system (CNS) and that the CPG driving neural activity of the motor neurons is located in the same brain area. Serotonergic neurons located in the nearby area of feeding related motor neurons project through the enteric nervous system to the gut. Functional analysis of these neurons revealed that brain derived serotonin plays a functional role in modulating foregut motility and we suggest that this serotonergic cluster consisting of four neurons is part of a brain-gut pathway functionally analogous to the mammalian vagus nerve. Manipulating the activity of other central neural populations expressing neuropeptides or neurotransmitters revealed that the different neural populations regulate all or distinct motor subprograms for feeding. Serotonergic neurons acted as general activator of all analyzed motor programs. Dopaminergic neurons and neurons expressing the Hugin neuropeptide inhibited specifically the motor pattern of the antennal nerve, whose efferent motor output is most dedicated to food intake by generating contractions of the cibarial dilator muscles (CDM).
The detailed analysis of the 20 Hugin neurons revealed that a subset of 16 cells (Hugin0.8) is responsible for the inhibition of food intake and wandering like behavior from an appetitive food source. The remaining four Hugin neurons (HuginVNC) were responsible for an increase in locomotive motor programs. Taken together, activation of the 20 Hugin neurons in the larval CNS leads to regulation of two mutually exclusive behaviors, inhibition of feeding and induction of locomotion. Having been proposed as gustatory interneurons earlier, we suggested that Hugin neurons act as bitter gustatory interneurons in the larval brain. This was verified by classical two-choice experiments, in which ablation of Hugin neurons resulted in animals no longer showing appropriate aversion to bitter substrates. With the generation of a specific Gal4 line, that exclusively labels eight Hugin neurons (HuginPC), projecting to the protocerebrum, it was possible to pinpoint observed effects of the Hugin neurons like feeding inhibition, wandering like behavior and impairment of bitter taste processing to these neurons. Using a new method of calcium imaging, called CaMPARI (Calcium Modulated Photoactivatable Ratiometric Integrator), we could show that the HuginPC neurons are selectively activated when larvae taste bitter substances. Furthermore, artificial activation of neurons expressing the bitter receptor GR66a led to rhythmic calcium activity in the HuginPC neurons. We suggest that the HuginPC neurons act as second order interneurons for bitter taste in Drosophila larvae. The mammalian homolog of Hugin is Neuromedin U (NMU). Pleiotropic roles have been assigned to this neuropeptide in regulating core biological processes like feeding and locomotion. Therefore, the new findings about the role of the Hugin neuropeptide might serve to gain insights into functional aspects of NMU regarding a role in taste processing.},

url = {http://hdl.handle.net/20.500.11811/6928}
}

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