UBC Theses and Dissertations
Dopamine and PDF signaling modulate habituation to repeated activation of a polymodal nociceptor in caenorhabditis elegans Ardiel, Evan
Habituation is a highly conserved phenomenon that remains poorly understood at the molecular level. Invertebrate model systems, like C. elegans, can be a powerful tool for understanding this fundamental process. To expand our knowledge of habituation I developed a high-throughput learning assay using real-time computer vision software for behavioral tracking and optogenetics for stimulation of a C. elegans polymodal nociceptor pair, ASHL and ASHR. These cells are especially interesting in the context of habituation because of the diversity and salience of the stimuli they detect. Photoactivation of ASH promoted backward locomotion and persistent stimulation altered the magnitude of this response in a manner consistent with the key behavioral characteristics of habituation. The decrement in reversal duration was readily reversed by a dishabituating stimulus, in this case non-localized mechanosensory input detected by the touch receptor neurons. In addition to altering the response properties, repeated ASH activation suppressed spontaneous reversals and accelerated forward movement. Food and dopamine signaling (bas-1, cat-4, cat-2, trp-4) promoted responding to persistent ASH activation and I identified the D1-like dopamine receptor, DOP-4, as the key mediator. Neuropeptide synthesis mutants (egl-3 and egl-21) displayed impaired plasticity for a variety of behavioral metrics, prompting me to perform an RNAi screen targeting neuropeptide receptors. From this screen, I implicated pigment dispersing factor (PDF) signaling in habituation of response latency and duration. Failure to avoid some stimuli detected by ASH could be fatal for C. elegans, so why do the reversal responses habituate? My data indicate that habituation is part of a strategy to promote dispersal.
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