Abstract
Behavioral and neuronal activity can be influenced by reward information through dopamine-modulated synaptic plasticity. Recent primate experiments (Lauereyns, Watanabe, Hikosaka 2002) using biased saccade task (BST) have demonstrated that the activity of caudate nucleus (CD) neurons are stronger and the behavioral responses are faster when the target of a saccadic eye movement indicates a reward than when it does not. It has been suggested that the observation can be explained by the following mechanism: The co-activation of the pre- and post synaptic neurons facilitates the synapses when dopamine is presented, but depresses the synapses when dopamine is absent (Hikosaka 2007; Hikosaka, Nakamura 2005). However, whether the proposed mechanism is sufficient to produce the observed behavioral and neuronal changes has not been tested. To address this problem, we built a spiking neural circuit model (Lo & Wang 2006) which includes a cortical module (Cx) that processes the visual stimulus, a basal ganglia module that employs the inhibitory control over eye movements and a superior colliculus module that drives the eye movements. By implementing the dopamine-induced plasticity in the cortico-striatal synapses, a pathway that has been shown to be a major target of dopaminergic neurons, we found that the previously proposed mechanism is not likely to be sufficient and additional neuronal interactions are needed for reproducing the observations. To address this issue, we propose a spick-timing dependent plasticity (STDP) mechanism based on the latest observations of STDP in the brain slices of rodent striatum. The proposed mechanism is able to reproduce the observations. We further explored the neural circuit model with several possible scenarios of synaptic dynamics and proposed experiments that might help to identify the detailed mechanism underlying the observed neuronal and behavioral changes in the biased reward condition.