Dopamine in motivational control - rewarding, aversive, and alerting: Midbrain dopamine neurons are well known for their strong responses to rewards and their critical role in positive motivation. It has become increasingly clear, however, that dopamine neurons also transmit signals related to salient but nonrewarding experiences such as aversive and alerting events. Here we review recent advances in understanding the reward and nonreward functions of dopamine. Based on this data, we propose that dopamine neurons come in multiple types that are connected with distinct brain networks and have distinct roles in motivational control. Some dopamine neurons encode motivational value, supporting brain networks for seeking, evaluation, and value learning. Others encode motivational salience, supporting brain networks for orienting, cognition, and general motivation. Both types of dopamine neurons are augmented by an alerting signal involved in rapid detection of potentially important sensory cues. We hypothesize that these dopaminergic pathways for value, salience, and alerting cooperate to support adaptive behavior. Dopamine-mediated learning and switching in cortico-striatal circuit explain behavioral changes in reinforcement learning: The basal ganglia are thought to play a crucial role in reinforcement learning. Central to the learning mechanism are dopamine (DA) D1 and D2 receptors located in the cortico-striatal synapses. However, it is still unclear how this DA-mediated synaptic plasticity is deployed and coordinated during reward-contingent behavioral changes. Here we propose a computational model of reinforcement learning that uses different thresholds of D1- and D2-mediated synaptic plasticity which are antagonized by DA-independent synaptic plasticity. A phasic increase in DA release caused by a larger-than-expected reward induces long-term potentiation (LTP) in the direct pathway, whereas a phasic decrease in DA release caused by a smaller-than-expected reward induces a cessation of long-term depression, leading to LTP in the indirect pathway. This learning mechanism can explain the robust behavioral adaptation observed in a location-reward-value-association task where the animal makes shorter latency saccades to reward locations. The changes in saccade latency become quicker as the monkey becomes more experienced. This behavior can be explained by a switching mechanism which activates the cortico-striatal circuit selectively. Our model also shows how D1- or D2-receptor blocking experiments affect selectively either reward or no-reward trials. The proposed mechanisms also explain the behavioral changes in Parkinsons disease. Cortico-basal ganglia mechanisms for overcoming innate, habitual and motivational behaviors: Most of the human behaviors are executed automatically under familiar circumstances. These behaviors are prepotent in that they take precedence over any other potential alternatives. Yet, humans are also capable of engaging cognitive resources to inhibit such a prepotent behavior and replace it with an alternative controlled behavior in response to an unforeseen situation. This remarkable capability to switch behaviors in a short period of time is the hallmark of executive functions. In this article, we first argue that the prepotent automaticity could emerge at least in three different domains - innate, habitual and motivational. We then review neurophysiological findings on how the brain might realize its switching functions in each domain, primarily by focusing on the monkey oculomotor system as the experimental model. Emerging evidence now suggests that multiple neuronal populations in the shared cortico-basal ganglia network contribute to overriding prepotent eye movement, be its origin innate, habitual or motivational. This consideration suggests the general versatility of the cortico-basal ganglia network as the neural mechanism whereby humans and other animals keep themselves from becoming subservient to reflex, habit and motivational impulses.
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