ArticleBehavioural brain research2015
Change in excitability of a putative decision-making neuron in Aplysia serves as a mechanism in the decision not to feed following food satiation.
Article in Behavioural brain research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Role of nitric oxide in the induction of the behavioral and cellular changes produced by a common aversive stimulus in Aplysia.Behavioural brain research · 2019Article
- cGMP mediates short- and long-term modulation of excitability in a decision-making neuron in Aplysia.Neuroscience letters · 2018Article
- Effects of internal and external factors on the budgeting between defensive and non-defensive responses in Aplysia.Behavioural brain research · 2018Article
- A novel in vitro analog expressing learning-induced cellular correlates in distinct neural circuits.Learning & memory (Cold Spring Harbor, N.Y.) · 2017Article
- Long-term sensitization training inLearning & memory (Cold Spring Harbor, N.Y.) · 2017Article
- Satiation level affects anti-predatory decisions in foraging juvenile crayfish.Journal of comparative physiology. A, Neuroethology, sensory, neural, and behavioral physiology · 2017Article
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Authors and funding
3 authors.
Funding
Abstract
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., 96 h 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.
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