Pacemaker potentials are the physiologic basis of epileptiform activity in the buccal ganglia of Helix pomatia

Mechanisms of epileptic activity in nervous systems were studied using the identified neurons B1 through B4 in the buccal ganglia of the snail Helix pomatia as a model system. Activities were recorded with intracellular microelectrodes. Epileptiform activity was induced by bath application of an epileptogenic drug (pentylenetetrazol: 1 mM to 40 mM, or etomidate: 0.1 mM to 1.0 mM). Epileptiform potentials recorded from the somata of neurons consisted of paroxysmal depolarization shifts (PDSs). With increasing concentration of an epileptogenic drug, pacemaker potentials in neuron B3 developed into PDS. Simultaneously several types of chemical post-synaptic potentials were suppressed in amplitude. Since on the one hand epileptic seizures only appear when PDS are synchronized in many neurons and since on the other hand synaptic potentials were found to be suppressed during epileptic conditions, mechanisms underlying neuronal synchronization were studied. Evidence was found that, under epileptogenic conditions only, neurons were synchronized by an non-synaptic release of substances. Strong depolarizations accompanied by an increase in intracellular calcium concentration are known to induce an unspecific exocytosis. Thus, an unspecific exocytosis from the dendrites of PDS-generating neurons probably appears under epileptic conditions and synchronizes neighbouring neurons.