These two abstracts are particularly interesting, with reference to the mechanisms for how rewards function in the brain and give rise to addiction- with obvious relationship to video gaming addiction. Video game developers actually hire neuroscientists to exploit these mechanisms to make games more addictive, and brain scans of heavy gamers are exactly the same as brain scans of other addicts because of mechanisms like this. I didn't know any of this when I saw my son go through withdrawal- but it goes a long way toward explaining it.
REWARD, PREDICTIONS AND UNCERTAINTY. W. Schultz*,Dept. of Anatomy, Univ. Cambridge, Cambridge, UK, CB2 3DY.
Survival in uncertain environments requires individuals to maximize the intake of liquid and food rewards.This task involves decision-making and goal-directed behavior which is based on the detection of rewards and the use of predictions for obtaining advance information and manging uncertainty. Based on learning theory and economic utility theory, we investigated the activity of individual neurons in major reward structures including the dopamine system, striatum and orbitofrontal cortex. We found that dopamine neurons detect the extent to which rewards occur differently than predicted, thus coding an 'error' in the prediction of reward. Together with their anatomical organization and influence on postsynaptic structures, dopamine responses may thus serve as explicit teaching signals for learning. Neurons in the orbitofrontal cortex discriminate well between different rewards irrespective of the positions and objects of the stimuli predicting them and may serve as a highly sensitive reward-discriminating system. Neurons in the striatum incorporate reward information into activity related to the preparation and execution of movements leading to the reward, thus reflecting a neural mechanism underlying goal-directed behavior. We then investigated how reward neurons in these structures code basic microeconomic decision variables and deal with uncertainty. Reward neurons are sensitive to the magnitude and probability of reward and their product (expected value). The neurons adapt their coding range and input-output gain to the uncertainty of rewards predicted by conditioned stimuli. In addition, dopamine neurons showa slower response that explicitly signals the uncertainty of reward, being maximal at a probability of 0.5 and covarying with the statistical variance. These data suggest that individual neurons process reward information in line with major theories of behavior and may be involved in managing the uncertainty involved in decision-making.
LEARNING AND PLASTICITY IN MOTIVATIONAL NETWORKS. A.E. Kelley*, University of Wisconsin-Madison Medical School, Madison, WI 53719-1176.
An important conceptual advance in the past decade hasbeen the understanding that the process of drug addiction shares striking commonalities with neural plasticity associated with natural reward learning and memory. Basic cellular mechanisms involving dopamine, glutamate, and their intracellular and genomic targets have been the focus of attention in the research areas of reward-related learning and addiction. These two neurotransmitter systems, widely distributed in many regions of cortex, limbic system and basal ganglia, appear to play a key integrative role in motivation, learning and memory. Coordinated neural signaling of dopaminergic and glutamatergic systems is a critical event in the induction of intracellular transcriptional and translational cascades, leading to alterations in gene expression andsynaptic plasticity, reconfiguration of neural networks, and ultimately learning of novel behaviors. Normally the brain uses these plasticity mechanisms, which have evolved within specialized neural circuits over millions of years of evolution, to optimize responses in organisms that ultimately enhance survival. However, many drugs of abuse exert their primary effects precisely on these pathways, and are apparently able to induce very long-term, perhaps even permanent, homeostatic alterations in motivational networks, thus leading to maladaptive behaviors.
Our own work shows that during learning of an instrumental task for food reward, DA-glutamate interactions in many corticolimbic areas lead to a constellation of molecular events involving induction of transcription factors and effector genes. There is also a dynamic shift in the pattern of gene expression (from prefrontal cortex to striatum) as animals progress from early action-outcome learning to highly skilled performance of a motor task. Moreover, we show that cues associated with both drugs of abuse and natural rewards (highly palatable food) exert powerful stimulus control over these circuits. These findings may provide clues to neuromolecular mechanisms underlying acquired motivation for drugs and energy-rich foods.
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