Event Abstract Back to Event Simulating Neural Network Development: Competition in Space and Time Influences the Formation of Neural Circuits Marcus Kaiser1* 1 Newcastle University, School of Computing Science, United Kingdom Introduction: The set of neural connections in the brain, or the connectome, is influenced by several factors including genetic information, self-organisation, physical constraints, and neural activity (learning and plasticity). Recent studies in Caenorhabditis elegans indicate that only 60% of the wiring organisation can be explained by gene expression patters indicating a major role of external factors. We use computer simulations to observe the effect of such developmental factors on the final network organisation (cf. http://www.biological-networks.org). On various spatial scales, from connectivity between individual neurons in C. elegans and rat visual cortex to connectivity between cortical areas in the mouse, macaque [1] and human brain, connection length distributions have very similar shapes, with a long flat tail representing the admixture of long-distance connections to mostly short-distance connections. Furthermore, not all potentially possible synapses are formed, and only a fraction of axons (called filling fraction, [2]) establish synapses with spatially neighbouring neurons. Results: Investigating local connectivity between individual neurons, we show that simple, random outgrowth of axons can reproduce distance-dependent connectivity as found in many neural systems [3]. Experimentally observed filling fractions can also be generated by competition for free space at the dendritic tree; a model markedly different from previous explanations. The filling fraction can be determined by the ratio between axon collaterals and free target sites which we call competition factor. The modeled filling fraction decays exponentially with the competition factor. Additional topological features, such as small-world organisation and modular systems can be derived by using multiple time windows [4]. Conclusion: Simple models that assume a random axonal outgrowth and competition for target space can account for the experimentally found exponential decay in the connection length distribution and the filling fraction. Acknowledgements: We thank the EPSRC (EP/E002331/1) and the Royal Society (RG/2006/R2) for financial support. INCF-09-88
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