Cellular mechanisms of decision making in Aplysia californica

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"A thesis submitted in partial fulfillment of the requirements for the degree of Master of Science in Biology."
All animals are perpetually besieged with stimuli and face an extraordinary array of choices. We constantly must decide to which stimuli to respond, as well as how and when to respond. Although the decision-making process is a fundamental brain function, understanding the mechanisms that govern this function is made difficult by the complexity of the brains of most animals. To overcome this obstacle, we studied Aplysia californica, a marine mollusk with a simple nervous system, whose behaviors are controlled by a limited number of identified and identifiable neurons. Aplysia feeding behavior offers the opportunity to study decision making at both the behavioral and cellular levels. Feeding behavior in Aplysia is critical for its survival and relies on characterized cells within the feeding neural circuit, which are amenable for cellular analysis. Aplysia exhibits biting movements to ingest food and, when food satiated, decides not to bite in the presence of food for a prolonged period of time (≥ 24 h; e.g., Kupfermann 1974a,b). Neuron B51, within the feeding neural circuit, exhibits decision-making characteristics, in that its all-or-nothing burst of activity biases the feeding neural circuit toward producing the motor patterns responsible for biting behavior (Nargeot et al. 1999; Brembs et al. 2002; Mozzachiodi et al. 2008). The goal of this study was to determine whether B51 is a site of plasticity underlying the decision not to bite following food satiation. The first objective of this study was to test the hypothesis that the satiation-induced decision not to bite is accompanied by a reduction in the activity of B51. Pairs of animals were used for each experiment, one experimental animal fed to satiation and one control animal kept unfed. The animal receiving satiation treatment was fed strips of seaweed until it decided to no longer bite in the presence of food. The effects of satiation on feeding behavior were analyzed using a seaweed extract to measure the number of bites. Seaweed extract was used to provide a constant food stimulus to elicit bites. Bites were measured before (pre-test) and 24 h after (post-test) treatment (satiation/control) to establish whether treatment caused any change in biting. The satiated group exhibited a significant decrease in the number of bites compared to the control group 24 h after treatment, which indicates the decision not to bite following food satiation was made in the satiated group. Cellular analysis of neuron B51 in satiated and control animals was possible because the effects of satiation persisted for 24 h. After the post-test, the buccal ganglia of satiated and control animals were isolated in vitro and B51 properties (resting membrane potential, input resistance and burst threshold) were measured. The satiated group exhibited a significantly higher burst threshold compared to the control group. B51 increase in burst threshold is indicative of a decrease in excitability, which is the function that enables neurons to generate action potentials in response to stimuli and is consistent with the suppression of feeding following satiation. No differences were observed in resting membrane potential or input resistance, which indicates that the decrease in B51 excitability induced by satiation treatment is intrinsic to the neuron. The second objective was to test the hypothesis that satiation-induced decreased excitability in B51 would no longer be observed at the time point in which biting resumed. Biting was no longer suppressed at 96 h following satiation (i.e., there was no significant difference in biting behavior between satiated and control animals). Notably, B51 excitability was not different between satiated and control animals 96 h after treatment. The experiments conducted addressed the function of decision making. We examined the cellular changes in the decision-making properties of neuron B51 following food satiation whereby the behavior controlled by this neuron is suppressed. In summary, these findings indicate that B51 is a site of plasticity underlying the decision not to bite following food satiation in Aplysia.
Life Sciences
College of Science and Engineering

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