Dopamine Model for Schizophrenia and Drug Addiction


Researchers have created a model that replicates how the brain releases dopamine.

researchers have created a model that replicates how the brain releases dopamine to help transmit signals between nerve cells. A result of an interdisciplinary collaboration, the model should prove to be an important tool in gaining an understanding of how people learn and how the brain perceives rewards and punishment.

Thus, the researchers, who published their results in October 20 issue of the Journal of Neuroscience, hope the model can be used in learning more about drug addiction and schizophrenia treatment; consumption of harmful narcotics results in a release of dopamine, which makes a person more likely to take that drug again, and researchers believe that such illnesses as schizophrenia are linked to imbalances of dopamine.

Indeed, actions that lead to a better-than-expected response result in a temporary release of more dopamine, whereas worse-than-expected responses have the opposite effect, with an actual halt in the release of dopamine. The process explains why we tend to repeat actions that result in high dopamine levels and avoid those that don’t.

"That's why many see dopamine as a learning signal," said co-creator of the model, Jakob Kisbye Dreyer, Department of Neuroscience and Pharmacology, Faculty of Health Sciences. "Others have argued that it is impossible for the dopamine system to react quickly enough to be a part of our learning process. It can take a split second to learn something, but a cell that releases dopamine works slowly. If you look at a lighthouse that flashes at a slow frequency, you might not notice right away that the light was turned off. Likewise, the arguments against dopamine as an aid to learning have focused on the slow feedback time when you experience something bad, and that it is too slow for the brain to make a connection. Our model shows that the collective signal from many cells provides a rapid enough reaction to influence learning."

Creation of the model was hampered because the study of active brains in living humans is highly difficult. "Theoretical neuroscience can easily become very complicated," said Dreyer. "If we try to come up with complete explanations of the way the brain works, we get models that are so complex that they are difficult to test." Thus, creation of the dopamine model was supported by observing animal models and the collaboration of physicists, mathematicians, and neurobiologists.

"Different branches of natural science have surprisingly different ways of thinking," said Dreyer. "Our work—and our model—is only possible because even though I am a physicist, I have been able to conduct research at the Department of Neuroscience and Pharmacology at the University of Copenhagen. As soon as we are certain that the model is correct, we can begin applying it to dopamine-related illnesses such as drug addiction and schizophrenia."

How far off do you think we are from seeing the impact of a dopamine model on the understanding of addiction and schizophrenia treatment? Do you think the model is flawed and thus can’t provide an accurate assessment of the role played by dopamine in the brain?

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