Synchronization of Synaptically Coupled Neural Oscillators

Abstract

The problem of epileptogenesis can be divided into two distinct but related components: the initiation of synchronous discharge, and its subsequent propagation. This division reflects clinical studies that suggest that a partial seizure originates in a localized area of cortex and either remains there or spreads to new areas. Moreover, an increasing number of experimental studies in vitro and in vivo suggest that the focus of seizure initiation involves a small fragment of a single cortical layer (possibly layer V) involving several thousand neurons that act as pacemaker cells (see [135] and references therein) . This synchronous activity then rapidly spreads vertically to encompass all other layers as well as propagating horizontally to recruit neighboring cortical areas [126] . Neuronal rhythmic activity also manifests itself in various aspects of normal brain function. For example, recent experimental observations indicate that synchronization and waves of excitation can occur in cortex during sensory processing [422,423] . Other systems supporting oscillations include the reticular thalamic nucleus (RTN), which is thought to act as a pacemaker for synchronous spindle oscillations observed during sleep or anesthesia [424,425] , the hippocampus [426] , and central pattern generators in locomotion [427]. The characteristics of local cortical circuits are of fundamental importance in understanding the origins of seizures.¹