Max Planck Institute for Dynamics and Self-Organization -- Department for Nonlinear Dynamics and Network Dynamics Group
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BCCN AG-Seminar

Thursday, 02.03.2006 16 s.t.

Computational neuroscience of homoeostatic plasticity - Modeling structural plasticity in prefrontal and hippocampal networks

by Markus Butz
from Universität Bielefeld


Seminarraum Haus 2, 4. Stock (Bunsenstr.)


Progressive and regressive events during development and in the mature brain are crucial for maintaining functional conditions in biological neural networks in a homoeostatic manner i.e. stabilizing neuronal activity. From increasing or decreasing synaptic receptor densities and altering synaptic efficiency over synthesizing and abolishing synaptic contacts up to cell proliferation and apoptosis etc., structural processes permanently reorganize the connectivity among nerve cells within mutually every part of the nervous system. In the mature brain, different regions show characteristic strategies of plasticity according to their functional needs. The dentate gyrus, entrance region of the hippocampal formation, shows a dramatic but functional reorganisation involving an ongoing synaptogenesis and cell turnover. In contrast, the prefrontal cortex shows a milder, predominantly synaptic reorganization. By the use of our computational modelling approach we are able to show that cell proliferation and synaptogenesis together contribute to a homoeostatic stability of hippocampal networks and enable them to adapt to a dramatically changing input spectrum via perforant path fibres. In other words, the proportion of new cells being synaptically integrated into a pre-existing network depend not only on the rate of cell proliferation alone, but also on the current activity of the network. Prefrontal networks, not endowed with cell turnover, suffer severe alterations of their connectivity pattern when affected by an adverse afference spectrum, i.e. a juvenile trauma or a pharmacological intoxication. Thus, the structural basis of a dysconnection syndrome as it can be seen in schizophrenia may relay on a common mechanism effecting activity-dependent plasticity in a functional and pathological situation.

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