title: Involvement of amygdala networks in epileptiform synchronization in vitro.
abstract: 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 microM) 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.
authors.affiliation: Montreal Neurological Institute and Departments of Neurology and Neurosurgery, and of Physiology, McGill University, Montreal, QC, H3A 2B4, Canada.
authors.forename: R
authors.initials: R
authors.lastname: Benini
authors.forename: M
authors.initials: M
authors.lastname: D'Antuono
authors.forename: E
authors.initials: E
authors.lastname: Pralong
authors.forename: M
authors.initials: M
authors.lastname: Avoli
mesh_terms: D015761:4-Aminopyridine / Q000494:pharmacology; D000200:Action Potentials / Q000187:drug effects / Q000502:physiology*; D000679:Amygdala / Q000187:drug effects / Q000502:physiology*; D000818:Animals; D008297:Male; D009415:Nerve Net / Q000187:drug effects / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D015761:4-Aminopyridine