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Every day, we encounter a flood of sensory information in our environment. How do we detect and discard irrelevant stimuli and how do we focus on the most salient features of our surroundings? Sensory thresholds are established and maintained through a variety of mechanisms, including a plasticity mechanism termed habituation. Habituation allows animals to dynamically increase their sensory thresholds, decreasing responsiveness to repeated, inconsequential stimuli.
Larval zebrafish are capable of detecting and responding to a wide variety of stimuli at 5 days post-fertilization. In particular, the acoustic startle response is a well-described, well-conserved, and robust behavior. In the fish, acoustic startle thresholds established during development can be modified through experience.
The Nelson Lab uses molecular-genetic, cell biological, and circuit-based techniques to identify how neural circuits develop and how they are modified to regulate sensory thresholds.
We have identified post-translational palmitoylation through the enzyme Zdhhc17/Hip14 as one critical mechanism underlying habituation of the acoustic startle response in larval zebrafish. We are now focused on identifying the relevant targets and where they act within the nervous system.
Our recent work has identified multiple loci within the nervous system that may be relevant for driving habituation learning. We are using calcium imaging and unbiased whole brain activity mapping to investigate whether and how activity within these neuronal populations changes during learning and how activity is disrupted in animals that cannot learn.
Discarding irrelevant stimuli is critical to the healthy functioning of the nervous system. So too is limiting plasticity in order to maintain appropriate behavioral thresholds. We have identified a handful of mechanisms that suppress habituation learning and now we are identifying where they act within the relevant circuitry.