Abstract
The role and organisation of the hippocampus not only gives us a unique opportunity to study the synaptic plasticity underlying LTP but also the changes in synaptic function associated with epilepsy. The kainic acid lesioned rat hippocampus has a pattern of cell loss that is similar to that found in temporal lobe epilepsy. In experiments using this chronic animal model of epilepsy we have observed changes in membrane and synaptic mechanisms that contribute to epileptiform bursting activity in the surviving CA1 pyramidal cells. The subject of this paper is to discuss the changes in inhibitory and excitatory synaptic function that underly this behaviour.
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