Motility of Dopamine and Serotonin-Deficient C. Elegans in Fed and Starved Conditions
Overview
The neurotransmitters dopamine and serotonin play important roles in animal nervous system function. Abnormal dopamine and serotonin signaling results in a variety of diseases and disorders, including ADHD, addiction, and Parkinson’s disease. The exact roles of dopamine and serotonin in the human brain, especially related to motor control, are not understood. Therefore, the goal of this research was to determine how defective dopamine and serotonin signaling in Caenorhabditis elegans affects locomotion rates. Locomotion enables C. elegans to seek out the bacteria they feed on to survive in the wild and in culture. In this experiment, wild-type, CBI 112 (cat-2) dopamine-deficient, and GRI 321 (tph-1) serotonin-deficient worms were chosen because these mutants have been seldom used in experiments relating to locomotion. Half of the worms in each strain were food-deprived for one hour, while the rest were fed a sufficient supply of their food, Escherichia coli OP50. After one hour, the worms were transferred to a plate that did or did not have E. coli OP50. The number of body bends of C. elegans were enumerated from 20 second digital recordings. Body bends were chosen as a more accurate representation of the worms’ locomotion rate, rather than speed of travel. The results suggest that food-deprived C. elegans that were introduced to seeded plates had fewer body bends during the observed 20 second periods than the worms subjected to other conditions. In addition, the fed worms that were introduced to seeded plates had fewer body bends than the worms introduced to unseeded plates. This suggests that, in the presence of E. coli, the worms slow down in response to entering a seeded plate.
Competition history
- AJAS 2019
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Source: AAAS Annual Meeting (Confex) / American Junior Academy of Science