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uni'wissen 01-2012_ENG

to as the gateway to the basal ganglia. The scien­ tists simulated an increased electrical activity in the striatum and, as a consequence, inhibited the globus pallidus more strongly. The result: The model shows the constant oscillation of elec­ trical activity of the two nerve cell networks in the basal ganglia that is characteristic of Parkin­ sonian patients. The striatum is thus a potential starting point for further research on the emer­ gence of Parkinson’s disease. However, the simu­ lation is a greatly reduced version of what actually happens in the brain. “In reality we have many more cells and a more complex network, but in principle, the model captures the main points of the brain’s behavior.” Kumar and his colleagues are also studying ways of improving DBS. The simulation led them to the conclusion that this method might require less electrical impulses than before in order to achieve a positive effect. “If we send the impulses at irregular intervals, we can leave up to 50 per­ cent of them out and still alleviate the symptoms.” That would save a whole lot of energy: The The computer model simulates the pulse-like activity of each individual neuron. The red points belong to the nerve cells of the subthalamic nucleus, the blue points to those of the globus pallidus. In a healthy person, the activity follows no apparent pattern. In Parkinson’s patients (gray bar) the cells of the two areas of the brain fall into rhythmic ­activity. The influence of deep brain stimulation (DBS, green bar) suppresses these oscillations. Dr. Arvind Kumar studied engineering at the Birla Institute of Technol- ogy and Science in Pilani, India, and neurobiology, biophysics, and compu­ tational neuroscience at the University of Freiburg. After completing his PhD in Freiburg he worked from 2006 to 2008 as a research assistant at the Department of Neurosciences of Brown University in Rhode Island, USA. Since 2008 he has served as a research group leader at the Bernstein Center Freiburg within the context of the program ­EuroSPIN (European Study Programme in Neuroinfor- matics), which combines neuroscience with computer science in order to reach a better understanding of the structure and function of the brain. His research ­interests include the dynam- ics of neuronal networks and the analysis and mod- eling of nerve cell activity. Further Reading Kumar, A./Aertsen, A. (2011): The role of ­inhibition in generating and controlling Parkin­ son’s disease oscillations in the basal ganglia. In: Frontiers in Systems Neuro­science 5/86. doi: 10.3389/fnsys.2011.00086 Moran, A./Stein, E./Tischler, H./Belelovsky, K./Bar-Gad, I. (2011): Dynamic stereotypic ­responses of basal ganglia neurons to sub­ thalamic nucleus high-frequency stimulation in the Parkinsonian primate. In: Frontiers in Systems Neuroscience 5/21. doi:10.3389/­ fnsys.2011.00021 Amtage, F. (2008): Tremor-correlated neuronal activity in the subthalamic nucleus of Parkin­ sonian patients. In: Neuroscience Letters 442/3, pp. 195 – 199. ­batteries of a neurostimulator in the brain would last longer, and they would not need to be ­replaced – which of course involves another ­operation – for eight years instead of four. Kumar stresses the importance of constant exchange with colleagues from medicine and the neurosciences, a collaboration which has also led to the joint proposal for the Cluster of Excel­ lence BrainLinks – BrainTools in Freiburg. He sees himself in the role of a creative director: “The theoretician plays the ball to the clinicians and gives them hints about what they could do to reach a better understanding of Parkinson’s ­disease.” For example, he recommends for ­researchers at hospitals and in private compa­ nies to take up the idea of improving DBS – and start developing and testing neurostimulators with a random impulse frequency that could function with half of the energy. “A green solution for DBS would be just the thing for a green city like Freiburg.” 19

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