Cerebral Cortex Advance Access originally published online on October 13, 2004
Cerebral Cortex 2005 15(6):834-845; doi:10.1093/cercor/bhh184
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Cerebral Cortex V 15 N 6 © Oxford University Press 2004; all rights reserved
Homeostatic Synaptic Plasticity Can Explain Post-traumatic Epileptogenesis in Chronically Isolated Neocortex
1 The Salk Institute, Computational Neurobiology Laboratory, La Jolla, CA 92037, USA, 2 Program in Neurosciences, University of California San Diego, La Jolla, CA 92093, USA, 3 Division of Biological Sciences, University of California San Diego, La Jolla, CA 92093, USA and 4 Laboratoire de Neurophysiologie, Université Laval, Québec, Canada G1K 7P4
Address correspondence to Arthur Houweling, Erasmus MC, Department of Neuroscience, Dr. Molewaterplein 50, 3015GE Rotterdam, The Netherlands. Email: arthur{at}salk.edu.
Chronically isolated neocortex develops chronic hyperexcitability and focal epileptogenesis in a period of days to weeks. The mechanisms operating in this model of post-traumatic epileptogenesis are not well understood. We hypothesized that the spontaneous burst discharges recorded in chronically isolated neocortex result from homeostatic plasticity (a mechanism generally assumed to stabilize neuronal activity) induced by low neuronal activity after deafferentation. To test this hypothesis we constructed computer models of neocortex incorporating a biologically based homeostatic plasticity rule that operates to maintain firing rates. After deafferentation, homeostatic upregulation of excitatory synapses on pyramidal cells, either with or without concurrent downregulation of inhibitory synapses or upregulation of intrinsic excitability, initiated slowly repeating burst discharges that closely resembled the epileptiform burst discharges recorded in chronically isolated neocortex. These burst discharges lasted a few hundred ms, propagated at 1–3 cm/s and consisted of large (10–15 mV) intracellular depolarizations topped by a small number of action potentials. Our results support a role for homeostatic synaptic plasticity as a novel mechanism of post-traumatic epileptogenesis.
Key Words: brain trauma • computational model • deafferentation • epilepsy • injury • slow oscillation
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