Abstract
The crustacean stomatogastric ganglion (STG) is a relatively simple central pattern generator that produces two well-studied robust rhythmic motor patterns in the absence of sensory feedback. One of the patterns, the pyloric rhythm, is responsible for controlling the muscles along the pyloric region of the crab’s stomach. Upstream neuromodulatory input from other ganglia support the pyloric rhythm by enhancing neuronal oscillations through an inward modulatory current (IMI).This modulation can be removed by a process called decentralization, which blocks/severs the connecting nerves. Previous studies have tested the response of the STG’s pyloric rhythm towards changes in ionic concentration, particularly 2.5x potassium concentration ([K+]) in its extracellular environment, which have led to the eventual crashing or silence of neural activity, followed by a gradual recovery. We are interested in understanding the role of upper neuromodulatory input in the circuit’s robustness and how its removal may affect how the pyloric rhythm adapts during repeated exposures to heightened levels of extracellular [K+]. Data provided by Mara Rue show that repeatedly exposing the circuit to a 2.5x [K+] environment, through 20-30 minute superfusions, causes the rhythm to consecutively increase its rate of recovery and decrease its chances of crashing. However, experiments that are decentralized before the repeated exposures have shown that removing upstream neuromodulatory input decreases the rhythm’s response recovery in 2.5x [K+], but does not eliminate the recovery altogether.