@article {2685, title = {Visual targeting of motor actions in climbing Drosophila.}, journal = {Current Biology}, volume = {20}, year = {2010}, month = {2010 Apr 13}, pages = {663-8}, abstract = {

Drosophila melanogaster flies cross surmountable gaps in their walkway of widths exceeding their body length with an astounding maneuver but avoid attempts at insurmountable gaps by visual width estimation. Different mutant lines affect specific aspects of this maneuver, indicating a high complexity and modularity of the underlying motor control. Here we report on two mutants, ocelliless(1) and tay bridge(1), that, although making a correct decision to climb, fail dramatically in aiming at the right direction. Both mutants show structural defects in the protocerebral bridge, a central complex neuropil formed like a handlebar spanning the brain hemispheres. The bridge has been implicated in step-length control in walking flies and celestial E-vector orientation in locusts. In rescue experiments using tay bridge(1) flies, the integrity of the bridge was reestablished, concomitantly leading to a significant improvement of their orientation at the gap. Although producing directional scatter, their attempts were clearly aimed at the landing site. However, this partial rescue was lost in these flies at a reduced-visibility landing site. We therefore conclude that the protocerebral bridge is an essential part of a visual targeting network that transmits directional clues to the motor output via a known projection system.

}, keywords = {Animals, Biological, Brain, Drosophila melanogaster, Genes, Genetically Modified, Insect, Models, Motor Activity, Mutation, Visual Perception}, issn = {1879-0445}, doi = {10.1016/j.cub.2010.02.055}, author = {Triphan, Tilman and Poeck, Burkhard and Neuser, Kirsa and Strauss, Roland} } @article {2689, title = {Analysis of a spatial orientation memory in Drosophila.}, journal = {Nature}, volume = {453}, year = {2008}, month = {2008 Jun 26}, pages = {1244-7}, abstract = {

Flexible goal-driven orientation requires that the position of a target be stored, especially in case the target moves out of sight. The capability to retain, recall and integrate such positional information into guiding behaviour has been summarized under the term spatial working memory. This kind of memory contains specific details of the presence that are not necessarily part of a long-term memory. Neurophysiological studies in primates indicate that sustained activity of neurons encodes the sensory information even though the object is no longer present. Furthermore they suggest that dopamine transmits the respective input to the prefrontal cortex, and simultaneous suppression by GABA spatially restricts this neuronal activity. Here we show that Drosophila melanogaster possesses a similar spatial memory during locomotion. Using a new detour setup, we show that flies can remember the position of an object for several seconds after it has been removed from their environment. In this setup, flies are temporarily lured away from the direction towards their hidden target, yet they are thereafter able to aim for their former target. Furthermore, we find that the GABAergic (stainable with antibodies against GABA) ring neurons of the ellipsoid body in the central brain are necessary and their plasticity is sufficient for a functional spatial orientation memory in flies. We also find that the protein kinase S6KII (ignorant) is required in a distinct subset of ring neurons to display this memory. Conditional expression of S6KII in these neurons only in adults can restore the loss of the orientation memory of the ignorant mutant. The S6KII signalling pathway therefore seems to be acutely required in the ring neurons for spatial orientation memory in flies.

}, keywords = {90-kDa, Animals, Drosophila melanogaster, gamma-Aminobutyric Acid, Locomotion, Memory, Models, Neurological, Neurons, Orientation, Ribosomal Protein S6 Kinases, Signal Transduction, Space Perception}, issn = {1476-4687}, doi = {10.1038/nature07003}, author = {Neuser, Kirsa and Triphan, Tilman and Mronz, Markus and Poeck, Burkhard and Strauss, Roland} } @article {2688, title = {Locomotor control by the central complex in Drosophila-an analysis of the tay bridge mutant.}, journal = {Developmental Neurobiology}, volume = {68}, year = {2008}, month = {2008 Jul}, pages = {1046-58}, abstract = {

Several aspects of locomotor control have been ascribed to the central complex of the insect brain; however, the role of distinct substructures of this complex is not well known. The tay bridge1 (tay1) mutant of Drosophila melanogaster was originally isolated on the basis of reduced walking speed and activity. In addition, tay1 is defective in the compensation of rotatory stimuli during walking and histologically, tay1 causes a mid-sagittal constriction of the protocerebral bridge, a constituent of the central complex. Cloning of the tay gene revealed that it encodes a novel protein with no significant homology to any known protein. To associate the behavioral phenotypes with the anatomical defect in the protocerebral bridge, we used different driver lines to express the tay cDNA in various neuronal subpopulations of the central brain in tay1-mutant flies. These experiments showed an association of the aberrant walking speed and activity with the structural defect in the protocerebral bridge. In contrast, the compensation of rotatory stimuli during walking was rescued without a restoration of the protocerebral bridge. The results of our differential rescue approach are supported by neuronal silencing experiments using conditional tetanus toxin expression in the same subset of neurons. These findings show for the first time that the walking speed and activity is controlled by different substructures of the central brain than the compensatory locomotion for rotatory stimuli.

}, keywords = {Amino Acid Sequence, Animal, Animals, Behavior, Brain, Cell Line, Drosophila melanogaster, Drosophila Proteins, Genetic Vectors, Locomotion, Male, Motor Activity, Mushroom Bodies, Mutation, Neurons, Phenotype, Photic Stimulation, Polymerase Chain Reaction, Transformed}, issn = {1932-8451}, doi = {10.1002/dneu.20643}, author = {Poeck, Burkhard and Triphan, Tilman and Neuser, Kirsa and Strauss, Roland} }