The final talk of the meeting was by my former postdoc supervisor John Byrne. He was talking about my favorite topic, obviously, operant conditioning in Aplysia. The preparation is great because the network is really well-known, the behavior is easy to observe and quantify and can be operantly and classically conditioned. It was a little weird to hear one's own data recounted by someone else
A central neuron in the buccal feeding CPG is the "decision-making neuron" B51. It fires a plateau potential late in the feeding cycle and only during ingestive behaviors. Depolarizing B51 increases ingestive programs and hyperpolarizing it reduces ingestion.
Operant conditioning is done by stimulating the esophageal nerve with electrical activity mimicking food delivery. Every time the animal bites, the nerve is stimulated. This leads to long term memory after only a few minutes of training. Studying B51 after training revealed an increased input resistance and decreased burst threshold in contingently reinforced animals compared to control animals. These results conform to results from B51 after in vitro conditioning of isolated buccal ganglia. Even experimentally induced changes in B51 alone lead to an increase in ingestive motor patterns. The B51 changes can also be observed if the neuron is taken in isolated cell culture and trained by depolarization and contingent dopamine application, indicating that the transmitter mediating reward is dopamine.
What happens inside of B51 to produce these significant changes? It turned out that cAMP is involved as well as PKC. It appears that the main intracellular convergence site of operant behavior and reward is an adenylate cyclase.