Abstract

Learning engages a high-dimensional neuronal population space spanning multiple brain regions. However, it remains unknown whether it is possible to identify a low-dimensional signature associated with operant conditioning, a ubiquitous form of learning in which animals learn from the consequences of behavior. Using single-neuron resolution voltage imaging, here we identify two low-dimensional motor modules in the neuronal population underlying Aplysia feeding. Our findings point to a temporal shift in module recruitment as the primary signature of operant learning. Our findings can help guide characterization of learning signatures in systems in which only a smaller fraction of the relevant neuronal population can be monitored.

Highlights

  • Learning engages a high-dimensional neuronal population space spanning multiple brain regions

  • An in vitro analog of operant conditioning (OC) has been developed by making electrical stimulation of esophageal nerve 2 (En2) contingent upon Buccal motor patterns (BMPs) occurring in the isolated ganglia

  • Direct stimulation of the dopamine-rich esophageal nerve 2 (En2), which acts as a reward, was made contingent upon ingestion-like BMPs

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Summary

Introduction

Learning engages a high-dimensional neuronal population space spanning multiple brain regions It remains unknown whether it is possible to identify a low-dimensional signature associated with operant conditioning, a ubiquitous form of learning in which animals learn from the consequences of behavior. It remains unknown whether it is possible to identify a low-dimensional “learning signature” associated with operant conditioning (OC), a ubiquitous form of learning in which an animal learns from the consequences of its behavior We addressed this question by leveraging the advantages of Aplysia feeding behavior. Buccal motor patterns (BMPs) of activity in these nerves correspond to protraction, retraction, and closure of the radula during in vivo feeding behavior[17]. Using in vivo and in vitro OC, some loci of nonsynaptic and synaptic plasticity engaged by OC have been characterized[22–24]

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