A Neural Network of Adaptively Timed Reinforcement Learning and Hippocampal Dynamics

A neural model is described of how adaptively timed reinforcement learning occurs. The adaptive timing circuit is suggested to exist in the hippocampus, and to involve convergence of dentate granule cells on CA3 pyramidal cells, and NMDA receptors. This circuit forms part of a model neural system for the coordinated control of recognition learning, reinforcement learning, and motor learning, whose properties clarify how an animal can learn to acquire a delayed reward. Behavioral and neural data are summarized in support of each processing stage of the system. The relevant anatomical sites are in thalamus, neocortex, hippocampus, hypothalamus, amygdala, and cerebellum. Cerebellar influences on motor learning are distinguished from hippocampal influences on adaptive timing of reinforcement learning. The model simulates how damage to the hippocampal formation disrupts adaptive timing, eliminates attentional blocking, and causes symptoms of medial temporal amnesia. It suggests how normal acquisition of subcortical emotional conditioning can occur after cortical ablation, even though extinction of emotional conditioning is retarded by cortical ablation. The model simulates how increasing the duration of an unconditioned stimulus increases the amplitude of emotional conditioning, but does not change adaptive timing; and how an increase in the intensity of a conditioned stimulus "speeds up the clock", but an increase in the intensity of an unconditioned stimulus does not. Computer simulations of the model fit parametric conditioning data, including a Weber law property and an inverted U property. Both primary and secondary adaptively timed conditioning are simulated, as are data concerning conditioning using multiple interstimulus intervals (ISIs), gradually or abruptly changing ISis, partial reinforcement, and multiple stimuli that lead to time-averaging of responses. Neurobiologically testable predictions are made to facilitate further tests of the model.

Cortical Dynamics of Feature Binding and Reset: Control of Visual Persistence

An analysis of the reset of visual cortical circuits responsible for the binding or segmentation of visual features into coherent visual forms yields a model that explains properties of visual persistence. The reset mechanisms prevent massive smearing or visual percepts in response to rapidly moving images. The model simulates relationships among psychophysical data showing inverse relations of persistence to flash luminance and duration, greaterr persistence of illusory contours than real contours, a U-shaped temporal function for persistence of illusory contours, a reduction of persistence: due to adaptation with a stimulus of like orientation, an increase or persistence due to adaptation with a stimulus of perpendicular orientation, and an increase of persistence with spatial separation of a masking stimulus. The model suggests that a combination of habituative, opponent, and endstopping mechanisms prevent smearing and limit persistence. Earlier work with the model has analyzed data about boundary formation, texture segregation, shape-from-shading, and figure-ground separation. Thus, several types of data support each model mechanism and new predictions are made.

The Role of Edges and Line-Ends in Illusory Contour Formation

Illusory contours can be induced along direction approximately collinear to edges or approximately perpendicular to the ends of lines. Using a rating scale procedure we explored the relation between the two types of inducers by systematically varying the thickness of inducing elements to result in varying amounts of "edge-like" or "line-like" induction. Inducers for our illusory figures consisted of concentric rings with arcs missing. Observers judged the clarity and brightness of illusory figures as the number of arcs, their thicknesses, and spacings were parametrically varied. Degree of clarity and amount of induced brightness were both found to be inverted-U functions of the number of arcs. These results mandate that any valid model of illusory contour formation must account for interference effects between parallel lines or between those neural units responsible for completion of boundary signals in directions perpendicular to the ends of thin lines. Line width was found to have an efFect on both clarity and brightness, a finding inconsistent with those models which employ only completion perpendicular to inducer orientation.