Amydgala Networks and Epileptiform Synchronization in the [italic]In Vitro [/italic] Limbic System.
Abstract number :
I.06
Submission category :
Year :
2001
Submission ID :
2307
Source :
www.aesnet.org
Presentation date :
12/1/2001 12:00:00 AM
Published date :
Dec 1, 2001, 06:00 AM
Authors :
E. Pralong, MD, Institute of Cellular Biology and Morphology, University of Lausanne, Lausanne, Switzerland; R. Benini, BSc, Neurology and Neurosurgery,and Physiology, Montreal Neurological Institute, McGill University, Montreal, QC, Canada; M. D[ssquote]
RATIONALE: The amygdala is at the origin of some behavioral manifestations in temporal lobe epilepsy and is the main limbic area used in the kindling model of epilepsy. Here we used horizontal rat brain slices to understand its involvement in epileptiform synchronization.
METHODS: Field potential recordings were made from slices containing the hippocampus, the entorhinal cortex (EC) and the basal amygdala during bath application of the convulsant drug 4-aminopyridine (4AP, 50[mu]M)
RESULTS: Brief epileptiform discharges originating in the CA3 area and propagated to all structures at intervals of 1.2-2.8 sec during 4AP application. These interictal-like discharges had duration of 454[plusminus]181 ms (n=12) when measured in CA3, and spread to the EC and the amygdala. Cutting the Schaffer collateral (n=12) abolished the propagation of the CA3-driven interictal activity to both EC and amygdala where robust interictal (duration=663[plusminus]512ms, n=12) and ictal discharges (duration= 15[plusminus]7 s, n=7) appeared. These two types of epileptiform activity could originate in either the EC or the amygdala (even in the same slice) and propagated to the CA3 via the perforant path. Cutting the connections between EC and the amygdala made independent interictal and ictal discharges appear in both structures. Electrical stimuli applied to the amygdala under control conditions elicited monosynaptic responses in the EC. Moreover, repetitive stimulation at frequencies [gte]0.5 Hz decreased and eventually blocked the ictal activity recorded in the EC (n=5).
CONCLUSIONS: CA3 outputs entrain EC and amygdala networks into a pattern of interictal activity that inhibits the occurrence of ictal discharges resembling electrographic limbic seizures that originate in either amygdala or EC. Moreover, after cutting the Schaffer collaterals, repetitive activation of amygdala inputs to EC control the ability of this limbic area to generate ictal discharges.
Support: CIHR
Disclosure: Grant - CIHR