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The role of GABA in modulating taste neuron output in Drosophila Chu, Bonnie


The sense of taste plays a critical role in animal behaviour. The ability to taste prior to ingestion allows an animal to differentiate between beneficial substances, such as calorie-rich foods, from those that may be toxic and which often taste bitter. For animals to avoid harmful substances, exposure to bitter substances must not only activate bitter-sensing neurons, but also suppress the response of acceptance-mediating neurons. The ability to choose appropriately between consumption and avoidance requires functional neuronal circuits in the brain that start with the processing of taste input from the environment and end with a behavioural output. γ-aminobutyric acid (GABA) is the primary inhibitory neurotransmitter in the insect and mammalian brain. We show evidence of functional connections between GABAergic interneurons (those that release GABA) and taste sensory neurons in the fly brain. Neurons that detect palatable substances (i.e. sugars) express high levels of a metabotropic GABAB receptor (GABABR), whereas those that sense unpalatable substances (i.e. bitter compounds) express little to no GABABR. Using a behavioural assay (proboscis extension reflex) and calcium imaging, I investigated how GABAergic inhibition shapes sweet neuron output and contributes to the integration of competitive taste stimuli. When GABABR is knocked down in sugar neurons, the behavioural response to sugars is elevated. Pharmacological assays show that GABAergic activation suppresses the sweet neuron response while GABAergic blockade potentiates the response. In flies expressing GABABR knockdown, suppression of sugar neuron activity by bitter exposure is relieved both behaviourally, by increased acceptance of bitter mixtures, and cellularly, by increased calcium response. Our model proposes that GABA acts via GABABR in the fly taste circuit to produce ecologically relevant responses to both attractive and repellent energy sources.

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