Optical recording of epileptiform voltage changes in the neocortical slice

Voltage sensitive probes were used to monitor the development, distribution, and spread of epileptiform potentials with a photodiode array in neocortical slices of guinea pigs. Epileptiform activity was induced by bath application of bicuculline-methiodide or 3,4-diaminopyridine and electrical stimulation of white matter or cortical layer I. Stimulation evoked a primary or early potential which was followed by a delayed epileptiform potential with a larger spatial extent. Shape, duration and amplitude of the delayed epileptiform potential varied strongly among slices and across the recording area and could reach largest amplitudes at a distance from the stimulation point. At a specific recording site, however, with repeated stimulation, potentials were generated in a stereotyped way. Intracellularly recorded delayed epileptiform potentials corresponded very closely at least to the early part of the optical response. Epileptiform activity appeared in layer III as soon as the primary potential reached sufficient amplitude there. Apart from this relationship, the distribution and spread of maximal amplitudes of delayed epileptiform potentials were segregated from those of early potentials. Early potentials reached maximal amplitudes close to the stimulation site. In contrast, the largest amplitudes of delayed epileptiform potentials were always found in layer III. A second maximum occasionally occurred in layer V. The horizontal amplitude distribution of epileptiform potentials was asymmetric, i.e. amplitudes increased to one side and decreased to the other. Early potential maxima spread from deeper to upper layers when initiated by white matter stimulation and from upper to deeper layers when initiated by layer I stimulation. In contrast, delayed epileptiform potentials always spread from layer III to lower layers and to the sides. Velocity of spread of early potentials and delayed epileptiform potentials differed systematically along the vertical and horizontal axis. The distribution of maximal amplitudes, shape, and pattern, of spread of epileptiform potentials was the same whether white matter or layer I was stimulated. The independence of delayed epileptiform potential characteristics from the point of stimulation and from early potential characteristics suggests that epileptiform activity is determined by intrinsic properties of the cortex and not by afferent activation.