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Homeostatic synaptic plasticity can explain post-traumatic epileptogenesis in chronically isolated neocortex.
Arthur R Houweling1, Maxim Bazhenov, Igor Timofeev
1The Salk Institute, Computational Neurobiology Laboratory, La Jolla, CA 92037, USA. arthur@salk.edu
Cerebral Cortex (New York, N.Y. : 1991)
|October 16, 2004
Summary
Homeostatic plasticity, a mechanism for stabilizing neuronal activity, may unexpectedly cause hyperexcitability and epileptogenesis in the brain after injury. This study reveals its role in post-traumatic epilepsy development.
Area of Science:
- Neuroscience
- Computational Neuroscience
- Epilepsy Research
Background:
- Chronically isolated neocortex exhibits hyperexcitability and epileptogenesis.
- The underlying mechanisms of post-traumatic epileptogenesis remain unclear.
- Homeostatic plasticity is typically viewed as a stabilizing mechanism.
Purpose of the Study:
- To investigate if homeostatic plasticity contributes to epileptogenesis in isolated neocortex.
- To model the effects of deafferentation-induced homeostatic plasticity on neuronal activity.
- To elucidate novel mechanisms of post-traumatic epilepsy.
Main Methods:
- Computer modeling of neocortex with a biologically based homeostatic plasticity rule.
- Simulating deafferentation and observing effects on neuronal firing rates and synaptic strength.
- Analyzing simulated burst discharges for characteristics matching experimental data.
Main Results:
- Simulated deafferentation induced homeostatic upregulation of excitatory synapses.
- This upregulation initiated slow, repeating burst discharges resembling epileptiform activity.
- The simulated bursts propagated at 1-3 cm/s with large depolarizations.
Conclusions:
- Homeostatic synaptic plasticity can paradoxically lead to hyperexcitability and burst firing.
- Homeostatic plasticity is a potential novel mechanism driving post-traumatic epileptogenesis.
- Findings challenge the view of homeostatic plasticity as solely a stabilizing process.