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Journal of Neuroscience, Vol 13, 4680-4689, Copyright © 1993 by Society for Neuroscience
Localized excitatory synaptic interactions mediate the sustained depolarization of electrographic seizures in developing hippocampus
JW Swann, KL Smith and RJ Brady
Cain Foundation Laboratories, Department of Pediatrics, Baylor College of Medicine, Houston, Texas 77030.
Repetitive synchronized neuronal discharging that lasts for seconds and
even minutes in in vitro brain slice preparations are important new models
in experimental epilepsy. In hippocampal slices from 1-2-week- old rats,
individual CA3 pyramidal cells undergo a sustained depolarization during
such electrographic seizures, induced by GABAA receptor antagonists. In
experiments reported here these events were produced in small isolated
segments of the CA3 subfield, measuring only 400-500 microns along the cell
body layer. In such minisclices local application of either kynurenic acid
or 6-cyano-7-nitroquinoxaline-2-3- dione (CNQX) to the proximal basilar
dendrites abolished the synchronized discharges of electrographic seizures.
Interictal spikes appeared unaffected by this treatment. Application of
these excitatory amino acid receptor antagonists to distal basilar
dendrites or apical dendrites was ineffective. In "larger" minislices,
measuring 700-1000 microns along the cell body layer, application of
kynurenic acid, CNQX, or TTX to the proximal basilar dendrites did not
abolish electrographic seizures but instead selectively suppressed the
intracellularly recorded sustained depolarization and the coincident slow
negative field potential recorded in proximal basilar dendrites. Results of
several experiments suggest that electrographic seizures recorded under
these conditions were produced by a remote network of "generator cells."
Since the remote neurons were unaffected by local application of the drugs,
it seemed likely that they continued to undergo a sustained depolarization.
Simultaneous blockade of basilar dendritic synapses in the "generator"
population abolished electrographic seizures throughout these larger
minislices. These results suggest that the sustained depolarization plays a
central role in seizure generation and that it does not have to be
generated in every neuron, only in a critical number of "generator cells"
for a seizure to occur. Taken together, results presented here suggest that
the sustained depolarization of electrographic seizures is a separate
physiological process from the more rapid repetitive depolarizations of the
seizure discharges and is required if electrographic seizures are to occur.
This slow depolarization appears to be synaptically mediated and generated
exclusively in proximal basilar dendrites. Therefore, in addition to the
excitatory synaptic potentials involved in paroxysmal depolarization shift
generation, a second form of recurrent excitation may exist in immature
hippocampus. Not only is this physiological process critical for the
genesis of seizures, but it also appears to be highly partitioned within
the hippocampal laminae.
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