Abstract
The enzyme, glycogen synthase kinase 3β (GSK3β), plays a key role in the development and maintenance of axons in neurons. Recent work has revealed microtubule (MT) unbundling in the axons of neurons with overactive or inactive GSK3β and it is hypothesised that this phenotype is tightly related to impaired axonal transport and synaptic defects. To test whether abnormal GSK3β activity affects neuronal function, the Drosophila visual system was probed using the steady-state visually evoked potential (SSVEP) technique. This involved recording electrophysiological responses from the fly eye presented with stimuli consisting of flickering light. Analyses revealed abnormal visual responses in flies expressing overactive or inactive GSK3β compared to control flies. To test whether this was due to MT unbundling, flies were fed with the MT-stabilising drug, Epothilone B (EpoB). The drug did not rescue the visual defects but instead led to adverse effects. Taken together, these results suggest that GSK3β dysregulation leads to neuronal dysfunction in the fly visual system, but MT unbundling may not be the sole mechanism underlying these visual defects.