Epileptic neurons induce augmenting synaptic depolarizations in non-epileptic neurons (buccal ganglia, Helix pomatia)

Abstract Spread of epileptic activity was studied by inducing epileptiform activity (pentylenetetrazol, PTZ) in one part of a nervous system and by analyzing responses of neurons in a non-PTZ-treated part (identified neurons, paired buccal ganglia, Helix pomatia ). Paroxysmal depolarization shifts (PDS) induced time-locked depolarizations in non-epileptic neurons (latency ca. 5 s, duration ca. 1 min, amplitude ≤20 mV). Amplitudes were augmenting during several hours of epileptic activity. Depolarizations were accompanied by an increase in membrane resistance and they were blocked in `high Mg-low Ca' solutions. It is assumed that the potentials represent a typical widespread response of non-epileptic neurons to PDS of other neurons. This response may be induced via non-specific releases of substances of the epileptically active neurons thereby activating neighboring neurons which in turn activate neurons in control ganglion.