Epileptiform activity in the guinea-pig neocortical slice spreads preferentially along supragranular layers--recordings with voltage-sensitive dyes.
The spread of epileptiform activity was monitored in guinea-pig neocortical slices by the use of a voltage-sensitive dye (RH795) and a fast optical recording technique. Epileptiform activity induced by bicuculline methiodide (10-20 microM) and single-pulse stimulation spread from the stimulation site in layer I or in the white matter across most of the slice. Different lesions were made in the slice in order to specify the neuronal connections used for spread in the horizontal direction. In the slice, intracortical connections are necessary for the spread of epileptiform activity, as shown by vertical cuts through all cortical layers but sparing the white matter. Horizontal connections were interrupted by cuts parallel to the axis of pyramidal neurons through either supragranular or infragranular layers. Vertical connections were interrupted by cuts perpendicular to the axis of pyramidal neurons separating supragranular and infragranular layers. Spread of epileptiform activity in the horizontal direction was not hindered by horizontal cuts. Vertical cuts through infragranular layers also did not hinder the spread of epileptiform activity. In contrast, vertical cuts through supragranular layers either abolished completely (nine slices) or delayed significantly (ten slices) the spread of epileptiform activity. The mean delay at the supragranular lesion was 44 ms in layer III and 30 ms in layer V; at the infragranular lesion the mean delay was 2 ms in layer III and 6 ms in layer V. Also, with horizontal cuts, in three out of five slices the velocity of spread was significantly lower in infragranular as compared to supragranular layers. It is concluded that both supra- and infragranular layers if isolated possess the ability to initiate and propagate epileptiform activity independently. However, in the intact slice the influence of the supragranular networks on initiation and propagation of epileptiform activity appears to dominate.
Albowitz
B
B
Department of Neurobiology, Max-Planck-Institute for Biophysical Chemistry, Göttingen, Germany.
Kuhnt
U
U
D000818:Animals; D001640:Bicuculline / Q000031:analogs & derivatives / Q000494:pharmacology; D002540:Cerebral Cortex / Q000187:drug effects / Q000503:physiopathology*; D003714:Denervation; D004558:Electric Stimulation; D004594:Electrophysiology; D004827:Epilepsy / Q000503:physiopathology*; D006168:Guinea Pigs; D009434:Neural Pathways / Q000503:physiopathology; D055095:Optics and Photonics; D013343:Styrenes
C096453:RH 795; D013343:Styrenes; C017069:bicuculline methiodide; D001640:Bicuculline