Tissue resistance changes and the profile of synchronized neuronal activity during ictal events in the low-calcium model of epilepsy.
Population spikes vary in size during prolonged epileptic ("ictal") discharges, indicating variations in neuronal synchronization. Here we investigate the role of changes in tissue electrical resistivity in this process. We used the rat hippocampal slice, low-Ca(2+) model of epilepsy and measured changes in pyramidal layer extracellular resistance during the course of electrographic seizures. During each burst, population spike frequency decreased, whereas amplitude and spatial synchronization increased; after the main discharge, there could be brief secondary discharges that, in contrast with those in the primary discharge, started with high-amplitude population spikes. Mean resistivity increased from 1,231 Omega.cm immediately before the burst to a maximum of 1,507 Omega.cm during the burst. There was no significant increase during the first 0.5-1 s of the field burst, but resistance then increased (tau approximately 5 s), reaching its peak at the end of the burst, and then decayed slowly (tau approximately 10 s). In further experiments, we modulated the efficacy of electrical field effects by changing perfusate osmolarity. Reducing osmolarity by 40-70 mOsm increased preburst resistivity by 19%; it reduced minimum population spike frequency (x0.6-0.7) and increased both maximum population spike amplitude (x1.5-2.3) and spatial synchronization (x1.4-2.5, cross-correlation over 0.5 mm) 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 synchronization of secondary discharges.
Department of Neurophysiology, The Medical School, Division of Neuroscience, University of Birmingham, United Kingdom.
John E
JE
Fox
Marom
M
Bikson
John G R
JG
Jefferys
D000200:Action Potentials / Q000187:drug effects / Q000502:physiology*; D000818:Animals; D002118:Calcium / Q000494:pharmacology* / Q000502:physiology; D004827:Epilepsy / Q000139:chemically induced / Q000503:physiopathology*; D006624:Hippocampus / Q000502:physiology; D066298:In Vitro Techniques; D008297:Male; D009474:Neurons / Q000187:drug effects / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley
D002118:Calcium