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Synaptic mechanisms underlying interictal spike initiation in a hippocampal network

IBM T.J. Watson Research Center (Dr. Traub), Yorktown Heights, NY, and Neurological Institute. New York, NY, and the Department of Physiology and Biophysics (Dr. Wong), University of Texas Medical Branch, Galveston, TX.

The intrinsic bursting capability of hippocampal neurons is well established. Recent experimental data also imply that CA3 neurons have mutual chemical excitatory interactions. Our previous simulations have shown how these two properties of the hippocampal CA3 region suffice to account for the synchronized burst discharges that occur in the presence of penicillin. Electrotonic interactions via gap junctions have also been described in the CA3 region, but their contribution to synchronization is not clear. We now show that a network of cells connected only by electrotonic junctions does not reproduce the experimental data on synchronization. In combination with chemical synapses, electrotonic junctions can prevent synchronized discharge, increase the degree of synchronization, or prolong the latency from stimulus to discharge. The effect electrotonic junctions have on synchronization of cellular bursting depends intimately on the density and strength of the chemical synapses.

Address correspondence and reprint requests to Dr. Traub, IBM Watson Research Center. Yorktown Heights, NY 10598.

An abstract of this work was presented to the American Academy of Neurology, Washington. DC, April 29, 1982.

Accepted for publication July 1, 1982.

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