Slow depolarizing potentials following penicillin-induced epileptiform bursting were recorded intracellularly from cat cortical neurons in vivo and guinea pig hippocampal neurons in vitro. In in vitro experiments, it was shown that blocking potassium conductance with tetraethylammonium resulted in epileptiform bursting and after potentials similar to those seen with penicillin application. It is hypothesized that an abnormality in potassium conductance, and a resulting increase in calcium influx, could be responsible for the long depolarizations characteristic of some neurons in epileptic foci.
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