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Classical conditioning (conventionally modeled as correlation-based learning) and operant conditioning (conventionally modeled as reinforcement learning or reward-based learning) have been found in biological systems. Evidence shows that these two mechanisms strongly involve learning about associations. Based on these biological findings, we propose a new learning model to achieve successful control policies for artificial systems. This model combines correlation-based learning using input correlation learning (ICO learning) and reward-based learning using continuous actor-critic reinforcement learning (RL), thereby working as a dual learner system. The model performance is evaluated by simulations of a cart-pole system as a dynamic motion control problem and a mobile robot system as a goal-directed behavior control problem. Results show that the model can strongly improve pole balancing control policy, i.e., it allows the controller to learn stabilizing the pole in the largest domain of initial conditions compared to the results obtained when using a single learning mechanism. This model can also find a successful control policy for goal-directed behavior, i.e., the robot can effectively learn to approach a given goal compared to its individual components. Thus, the study pursued here sharpens our understanding of how two different learning mechanisms can be combined and complement each other for solving complex tasks. [ABSTRACT FROM AUTHOR]

In this theoretical contribution, we provide mathematical proof that two of the most important classes of network learning—correlation-based differential Hebbian learning and reward-based temporal difference learning—are asymptotically equivalent when timing the learning with a modulatory signal. This opens the opportunity to consistently reformulate most of the abstract reinforcement learning framework from a correlation-based perspective more closely related to the biophysics of neurons. [ABSTRACT FROM AUTHOR]

Abstract: It has been shown that plasticity is not a fixed property but, in fact, changes depending on the location of the synapse on the neuron and/or changes of biophysical parameters. Here, we investigate how plasticity is shaped by feedback inhibition in a cortical microcircuit. We use a differential Hebbian learning rule to model spike-timing-dependent plasticity and show analytically that the feedback inhibition shortens the time window for LTD during spike-timing-dependent plasticity but not for LTP. We then use a realistic GENESIS model to test two hypothesis about interneuron hypofunction and conclude that a reduction in GAD67 is the most likely candidate as the cause for hypofrontality as observed in Schizophrenia. [Copyright &y& Elsevier]