Selective degeneration and synaptic reorganization of hippocampal interneurons in a chronic model of temporal lobe epilepsy.

Abstract

Synaptic properties and connectivity of GABAergic inhibitory interneurons are modified in CA1 hippocampus of the KA model of epilepsy (Fig. 1). These changes affect interneurons that target dendritic areas of principal cells and have important consequences for network activity and hyperexcitability. Some of these changes contribute to hyperexcitability, while others likely develop to compensate for the hyperexcitability of the network. However, some of these "compensatory" changes might also paradoxically contribute to hyperexcitability and epileptogenesis.