| Autor: |
Poppinga H; Department of Molecular Neurobiology of Behaviour, University of Göttingen, Julia-Lermontowa-Weg 3, 37077 Göttingen, Germany., Çoban B; Department of Molecular Neurobiology of Behaviour, University of Göttingen, Julia-Lermontowa-Weg 3, 37077 Göttingen, Germany., Meltzer H; Departments for Molecular Cell Biology and Molecular Neuroscience, Weizmann Institute of Science, Ullmann Building of Life Sciences, Rehovot 7610001, Israel., Mayseless O; Departments for Molecular Cell Biology and Molecular Neuroscience, Weizmann Institute of Science, Ullmann Building of Life Sciences, Rehovot 7610001, Israel., Widmann A; Department of Molecular Neurobiology of Behaviour, University of Göttingen, Julia-Lermontowa-Weg 3, 37077 Göttingen, Germany., Schuldiner O; Departments for Molecular Cell Biology and Molecular Neuroscience, Weizmann Institute of Science, Ullmann Building of Life Sciences, Rehovot 7610001, Israel., Fiala A; Department of Molecular Neurobiology of Behaviour, University of Göttingen, Julia-Lermontowa-Weg 3, 37077 Göttingen, Germany. |
| Abstrakt: |
The principles of how brain circuits establish themselves during development are largely conserved across animal species. Connections made during embryonic development that are appropriate for an early life stage are frequently remodelled later in ontogeny via pruning and subsequent regrowth to generate adult-specific connectivity. The mushroom body of the fruit fly Drosophila melanogaster is a well-established model circuit for examining the cellular mechanisms underlying neurite remodelling. This central brain circuit integrates sensory information with learned and innate valences to adaptively instruct behavioural decisions. Thereby, the mushroom body organizes adaptive behaviour, such as associative learning. However, little is known about the specific aspects of behaviour that require mushroom body remodelling. Here, we used genetic interventions to prevent the intrinsic neurons of the larval mushroom body (γ-type Kenyon cells) from remodelling. We asked to what degree remodelling deficits resulted in impaired behaviour. We found that deficits caused hyperactivity and mild impairment in differential aversive olfactory learning, but not appetitive learning. Maintenance of circadian rhythm and sleep were not affected. We conclude that neurite pruning and regrowth of γ-type Kenyon cells is not required for the establishment of circuits that mediate associative odour learning per se , but it does improve distinct learning tasks. |
