The dentate gyrus as a regulated gate for the propagation of epileptiform activity.

Properties of the interaction between the entorhinal cortex (EC) and the dentate gyrus were studied in a combined EC hippocampal slice preparation in which most of the fiber connectivity within this structure is intact. Epileptiform activity was induced by lowering extracellular Mg2+ concentration. This caused short recurrent discharges in the hippocampus while seizure-like events (SLE) slowly spread from the site of initiation to neighboring areas. At the end of a SLE, the EC, the subiculum and the neocortical area Te2 discharged in synchrony. This activity could develop into a state of recurrent tonic discharges highly synchronized between the different areas. These discharges were insensitive to treatment with currently available antiepileptic drugs. Although the SLE increased neuronal firing and extracellular potassium concentration in the dentate gyrus, this activity had only moderate effects on the activity generated in areas CA3 and CA1. Removing GABAergic inhibition with baclofen and bicuculline caused the spread of SLE from the EC to the dentate gyrus. Slow inhibitory postsynaptic potentials and intrinsic properties of dentate gyrus granule cells appear to underlie the filtering function of the dentate gyrus.