Abstract
Epileptic seizures are based on paroxysmal depolarization shifts (PDS) which are synchronized in many neurons. Mechanisms underlying PDS and seizures are still not understood. The present review is based on studies using the buccal ganglia of the snail Helix pomatia as a model nervous system. Essential mechanisms of epileptic activity in nervous systems are thought to be identical in whatever part of the human or animal nervous system epileptic activity appears. From studies using the buccal ganglia of Helix pomatia, epileptic activity is essentially non-synaptic. PDS are “giant pacemaker potentials”, which are generated non-synaptically by the single neurons. It is, however, not yet clear which processes transform pacemaker potentials into PDS. Synchronization of PDS follows generation of PDS and results mainly from a non-synaptic, unspecific release of intracellular substances from the dendrites of a PDS-generating neuron to the dendrites of neighbouring neurons. This explains the existence of small epileptic foci. From the above observations epileptogenicity is introduced or intensified when the proteins underlying pacemaker potentials are expressed. The first chapter of the present review presents the model system. The second chapter describes epileptiform activity in the model system to correspond in all aspects to epileptiform activity recorded in vertebrate nervous systems including man. Subsequently, antiepileptic and epileptogenic properties of drugs are described using the buccal ganglia. Two following chapters concern neuronal structures and neuronal functions affected by epileptiform activity, and in the final chapter the mechanisms underlying epileptiform activities are described.
Keywords: epileptic activity, epileptogenicity, model nervous system, pacemaker potential, synchronization of epileptic activity, non-synaptic release, synaptic potentials, antiepileptic drugs
