Biophysical and molecular mechanisms of mean and variance adaptation in the Drosophila ear

Abstract

Adaptation is an important mechanism found across sensory systems and species. This important ability of sensory systems expands our range of perception. Giving us the ability to perceive a quiet whisper as well as a loud heavy metal concert. For many receptors, adaptation is well described, but often their underlying mechanisms are still poorly understood. For example in the case for the auditory receptor of Drosophila melanogaster. Two forms of adaptation happen in the auditory sensory system of the fly. First, an adaptation to the slow changing mean of a stimulus, called offset or mean adaptation. Secondly, an adaptation to the faster changing intensity of the stimulus, commonly referred to as intensity or variance adaptation. In this thesis we explored the mechanisms underlying the different forms of adaptation in the primary auditory receptor neurons (Johnston's organ neurons) of the fruit fly, by screening candidate mutant fly strains. The choice of candidates were based on their expression in the Johnston's organ neurons and a hypothetical way the molecule could induce adaptation. In total we screened 17 different mutant strains, including mutations of K+ channels, motor proteins and small GTPases and characterized adaptation in these mutants. Current clamp recordings of compound action potentials from the Johnston's organ neurons were used to access the adaptation properties of the fruit fly and their change induced by certain mutations. We recorded reduced speed and strength of variance adaptation in six different mutants, including mutations of eag, rgk1 and dynein. The most prominent effects could be measured in the mutations of eag. While the Eag channel is known to be mediated by Ca2+ via Calmodulin, we did not observe any effect of mutations interfering with this Eag/Ca2+ interaction, suggesting that this process is insignificant for adaptation. Furthermore, while this K+ channel mutant influenced variance adaptation, it did not influence mean adaptation properties. We found evidence that the Eag channel is part of the molecular mechanism of variance adaptation, but not involved in mean adaptation. The mutations affecting variance adaptation in general did not affect mean adaptation. This corroborates the hypothesis that different mechanisms are involved in these two types of adaptation in the fly.