Population spikes vary in size during prolonged epileptic ("ictal") discharges, indicating variations in neuronal synchronisation. Here we investigate the role of changes in tissue electrical resistivity in this process. We used the rat hippocampal slice, low Ca²⁺ model of epilepsy and neasured changes in pyramidal layer extracellular resistance during the course of electrographic seizures. During each burst, population spike frequency decreased, while amplitude and spatial synchronisation increased; following the main discharge, there could be brief secondary discharges in which, by contrast with those in the primary discharge, started with high amplitude population spikes. Mean resistivity increased from 1231 .cm immediately before the burst to a maximum of 1507 .cm during the burst. There was no significant increase during the first 0.5 to 1 s of the field burst, but resistance then increased (~5 s), reaching its peak at the end of the burst, and then decayed slowly (~10 s). In further experiments, we modulated the efficacy of electrical field effects by changing perfusate osmolarity. Reducing osmolarity by 40 to 70 mOsm increased preburst resistivity by 19%; it reduced minimum population spike frequency (x 0.6-0.7) and increased both maximum population spike amplitude (x 1.5-2.3) and spatial synchronization (x 1.4-2.5, cross-correlation over 0.5mm) during bursts. Increasing osmolarity by 20-40 mOsm had the opposite effects. These results suggest that, during each field burst, field effects between neurons gradually become more effective, as cells swell, thereby modulating burst dynamics and facilitating the rapid synchronisation of secondary discharges.