Abstracts

RATIONALE: Low calcium field bursts consist of a spontaneous 10-15 sec negative shift in potential, superimposed on which are rhythmic, 20-50 Hz population spike discharges which are interrupted for variable periods during the burst; the purpose of the present investigation was to identify factors that contribute to the interruption of population spike discharges.
METHODS: Extracellular (population potentials) and intracellular recordings were made from the CA1 region of the rat hippocampal slice, maintained in an interface chamber. Slices were perfused with artificial CSF in which potassium concentration was increased to 5 mM and calcium concentration reduced to 0.2 mM.
RESULTS: Field bursts were classified into types I-III, depending on whether population spikes were present for 90-100%, 10-90% or 0-10% of the event. A possible mechanism which could cause the interruption in population spike generation during the field bursts is desynchronisation of action potentials in individual neurons. To investigate this question, simultaneous field and intracellular recordings were made; our results showed that when population potentials were absent during an ictal burst, action potential generation in individual neurons was interrupted rather than desynchronised. Moreover, intracellular recordings showed that, during type III bursts, although neurons produced action potentials only for brief periods at the beginning and end of the field burst, they were depolarised throughout the event. In a further group of experiments, current was passed through the intracellular electrode, hyperpolarising the neuron during the ictal event. The effect of this hyperpolarisation was to induce action potential firing, so that 20-50 Hz spikes could again be seen.
CONCLUSIONS: The experiments demonstrate that depolarisation block has a role in blocking action potential discharge in individual neurons and therefore in interrupting population spike discharges in the low calcium model of epilepsy. Patients with focal epilepsy sometimes demonstrate a localised electrodecremental event prior to the onset of a seizure. These events are characterised by a reduction of background EEG activity accompanied or followed by a period of low amplitude 20-50Hz rhythmic sinusoidal activity and we speculate that the depolarisation block, demonstrated in the present experiments, could play a role in generating these localised electrodecremental events in human epilepsy.
[Supported by: MRC (UK)]