Introduction

The balance between excitatory and inhibitory synaptic transmission is often considered as potentially one of the most important mechanisms for initiation of epileptic seizures. One example of this synaptic balance is the cerebral cortex where feedback and feedforward inhibition regulate the spread of excitatory pyramidal neuron firing (Benardo and Wong, 1995). Experimental studies suggest that modification of inhibitory transmission in neural circuits influences overall neuronal activity, leads to burst firing in neurons and subsequent propagation of epileptiform activity in networks. In vitro experimental models produce reduced inhibition by applying convulsant agents (e.g. penicillin, picrotoxin, bicuculline) that block inhibitory receptors.

The phenomenon of synchronous bursting may be easily studied theoretically in simulated neural networks of excitatory and inhibitory neurons. Computer simulation allows one to more exactly (than using in vitro or in situ models) evaluate the role of decreasing inhibition in promoting increased synchronous activity in neural networks. In the experiments presented here we consider realistic locally connected small neural networks (up to 36 neurons) using the Rinzel/Av Ron (Rinzel 1985, Av Ron 1994) neuron model. We show how such small networks can become epileptic networks as a result of changing network parameters. Specifically we show how relative changes in synaptic inhibition and excitation contribute to increased network synchronization and organized bursting activity.