Optogenetic and pharmacologic dissection of feedforward inhibition in Drosophila motion vision

• Published in: The Journal of neuroscience 2014-02, Vol.34 (6), p.2254-2263
• Main Authors: Mauss, Alex S, Meier, Matthias, Serbe, Etienne, Borst, Alexander
• Format: Article
• Language: English
• Subjects: Animals; Drosophila; Female; Mecamylamine - pharmacology; Motion Perception - drug effects; Motion Perception - physiology; Neural Inhibition - drug effects; Neural Inhibition - physiology; Optogenetics - methods; Photic Stimulation - methods; Picrotoxin - pharmacology; Vision, Ocular - drug effects; Vision, Ocular - physiology; Visual Pathways - drug effects; Visual Pathways - physiology
• ISSN: 0270-6474; 1529-2401
• DOI: 10.1523/JNEUROSCI.3938-13.2014

Visual systems extract directional motion information from spatiotemporal luminance changes on the retina. An algorithmic model, the Reichardt detector, accounts for this by multiplying adjacent inputs after asymmetric temporal filtering. The outputs of two mirror-symmetrical units tuned to opposite directions are thought to be subtracted on the dendrites of wide-field motion-sensitive lobula plate tangential cells by antagonistic transmitter systems. In Drosophila, small-field T4/T5 cells carry visual motion information to the tangential cells that are depolarized during preferred and hyperpolarized during null direction motion. While preferred direction input is likely provided by excitation from T4/T5 terminals, the origin of null direction inhibition is unclear. Probing the connectivity between T4/T5 and tangential cells in Drosophila using a combination of optogenetics, electrophysiology, and pharmacology, we found a direct excitatory as well as an indirect inhibitory component. This suggests that the null direction response is caused by feedforward inhibition via yet unidentified neurons.