Spread of epileptic activity was studied by inducing epileptiform acti
vity (pentylenetetrazol, PTZ) in one part of a nervous system and by a
nalyzing responses of neurons in a non-PTZ-treated part (identified ne
urons, paired buccal ganglia, Helix pomatia). Paroxysmal depolarizatio
n shifts (PDS) induced time-locked depolarizations in non-epileptic ne
urons (latency ca. 5 s, duration ca. 1 min, amplitude less than or equ
al to 20 mV). Amplitudes were augmenting during several hours of epile
ptic activity. Depolarizations were accompanied by an increase in memb
rane resistance and they were blocked in 'high Mg-low Ca' solutions. I
t is assumed that the potentials represent a typical widespread respon
se of non-epileptic neurons to PDS of other neurons. This response may
be induced via non-specific releases of substances of the epileptical
ly active neurons thereby activating neighboring neurons which in turn
activate neurons in control ganglion. (C) 1997 Elsevier Science Irela
nd Ltd.