Paroxysmal depolarization shifts (PDS) induce non-synaptic responses in neighboured neurons (buccal ganglia, Helix pomatia).

A non-synaptic spread of excitation between neighboured neurons was studied in a model nervous system using epileptiform activity. The identified giant neuron B3 in the buccal ganglia of Helix pomatia reliably generated paroxysmal depolarization shifts (PDS) when treated with pentylenetetrazol or etomidate. Simultaneous recordings of neuron B3 and other neurons showed that each PDS in neuron B3 was accompanied by a depolarization in the other neurons. These related depolarizations (PDS-RD) appeared about 1 to 5 s after the beginning of PDS, their amplitude was up to 20 mV and their duration ca. 1 min. Reduction of extracellular calcium concentration or application of a "high Mg-low Ca" solution blocked PDS-RD. There were, however, no hints for synaptic contacts of the studied neurons. Occasional failures of spontaneous PDS in one neuron B3 of the B3-network of neurons, resulted in a failure of PDS-RD in the neighboured neurons. Block and induction of PDS in one neuron by injection of hyperpolarizing and depolarizing currents, respectively, blocked and induced PDS-RD in the neighboured neurons. As intracellular staining of neurons B1 and B3 showed that their dendritic arborizations were co-localized in the same region of the ganglion, a dendro-dendritic release of substances may cause PDS-RD. Since PDS-RD could themselves trigger PDS, PDS-RD may provide a new basic mechanism of synchronizing epileptic activity of neighboured neurons within an epileptic focus.