What, exactly, was wrong with the Hawkins and Kandel model of learning in Aplysia?
What remedies were proposed? Answer: Hawkins and Kandel attempted to show how simple non-associative mechanisms could reproduce a variety of classical conditioning effects in Aplysia. In their model, neurons coding for CSes and the US make synapses onto both a motor neuron (MN) that could produce CRs, and a facilitory interneuron (FI). The CS synapses are initially weak; the US synapses are strong. The FI makes synapses onto the CS unit’s synapses, both those on the motor neuron and those on the FI. When the FI fires, it strengthens the weights of any CS synapses that were recently active — within a certain time window. When CS1 is paired with the US in training, the CS1 activity is usually not enough to fire the FI or MN. The US that follows fires both the MN, producing a UR, and the FI, which strengthens the CS1-MN and CS1-FI connections. With repeated pairings, the CS1 connection becomes strong enough to trigger the MN on its own, thus producing a CR. CS1-US pairings also cause the
