Involvement of amygdala networks in epileptiform synchronization in vitro

We used field potential and intracellular recordings in rat brain slices that included the hippocampus, a portion of the basolateral/lateral nuclei of the amygdala (BLA) and the entorhinal cortex (EC). Bath application of the convulsant 4-aminopyridine (50 μM) to slices (n=12) with reciprocally connected areas, induced short-lasting interictal-like epileptiform discharges that (i) occurred at intervals of 1.2–2.8 s, (ii) originated in CA3, and (iii) spread to EC and BLA. Cutting the Schaffer collaterals abolished them in both parahippocampal areas where slower interictal-like (interval of occurrence=4–17 s) and prolonged ictal-like discharges (duration=15±6.9 s, mean±S.D., n=7) appeared. These new types of epileptiform activity originated in either EC or BLA. Similar findings were obtained in slices (n=19) in which the hippocampus outputs were not connected with the EC and BLA under control conditions. Cutting the EC–BLA connections made independent slow interictal- and ictal-like activities appear in both areas (n=5). NMDA receptor antagonism (n=6) abolished ictal-like discharges and reduced the duration of the slow interictal-like events. Repetitive stimulation of BLA at 0.5–1 Hz in Schaffer collateral cut slices, induced interictal-like epileptiform depolarizations in EC and reversibly blocked ictal-like activity (n=14). Thus, CA3 outputs in intact slices entrain EC and BLA networks into an interictal-like pattern that inhibits the propensity of these parahippocampal areas to generate prolonged ictal-like paroxysms. Accordingly, NMDA receptor-dependent ictal-like events are initiated in BLA or EC once the propagation of CA3-driven interictal-like discharges to these areas is abated by cutting the Schaffer collaterals. Similar inhibitory effects also occur by activating BLA outputs directed to EC at rates that mimic the CA3-driven interictal-like pattern. [Copyright &y& Elsevier]