Change in excitability of a putative decision-making neuron in Aplysia serves as a mechanism in the decision not to feed following food satiation

• Published in: Behavioural brain research 2015-03, Vol.281, p.131-136
• Main Authors: Dickinson, Kathy J., Wainwright, Marcy L., Mozzachiodi, Riccardo
• Format: Article
• Language: English
• Subjects: Animals; Aplysia; Bites and Stings - psychology; Decision making; Decision Making - physiology; Excitability; Excitatory Postsynaptic Potentials - physiology; Feeding; Feeding Behavior - physiology; Feeding Behavior - psychology; Mollusca; Neurons - physiology; Nonsynaptic plasticity; Satiation; Satiation - physiology; Time Factors
• ISSN: 0166-4328; 1872-7549
• DOI: 10.1016/j.bbr.2014.12.022

•We examined the mechanisms of the decision not to feed after satiation in Aplysia.•The decision not to feed was accompanied by decreased excitability of neuron B51.•The decrease of B51 excitability was not observed once feeding had resumed.•Changes in B51 excitability contribute to the decision not to feed after satiation. Although decision making is a ubiquitous function, the understanding of its underlying mechanisms remains limited, particularly at the single-cell level. In this study, we used the decision not to feed that follows satiation in the marine mollusk Aplysia to examine the role of putative decision-making neuron B51 in this process. B51 is a neuron in the feeding neural circuit that exhibits decision-making characteristics in vitro, which bias the circuit toward producing the motor programs responsible for biting behavior. Once satiated, Aplysia decided not to bite for a prolonged period of time (≥24h) when presented with a food stimulus that normally elicits feeding in non-satiated animals. Twenty-four hours after satiation, suppressed feeding was accompanied by a significant decrease of B51 excitability compared to the control group of unfed animals. No differences were measured in B51 resting membrane properties or synaptic input to B51 between the satiated and control groups. When B51 properties were measured at a time point in which feeding had recovered from the suppressive effects of satiation (i.e., 96h after satiation), no difference in B51 excitability was observed between satiated and control groups. These findings indicate that B51 excitability changes in a manner that is coherent with the modifications in biting resulting from food satiation, thus implicating this neuron as a site of plasticity underlying the decision not to bite following food satiation in Aplysia.