Address correspondence and reprint requests to Dr. S. Kogure at Department of Bioengineering, Faculty of Engineering, Soka University, 1-236 Tangi-cho, Hachioji, Tokyo 192-8577, Japan. E-mail: [email protected]

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Abstract

Summary: Purpose: Alternate-site kindling (AK), which has been known to induce so-called kindling antagonism, was performed in the bilateral hippocampi to reveal neural mechanisms underlying hippocampal kindling.

Methods: Ten adult rabbits were used. Daily kindling stimulation consisted of a 1- s train of 50 pulses (pulse duration, 1 ms) of 80 to 200 μA (base-to-peak), which was higher than the afterdischarge (AD) threshold. The concurrent alternating stimulations were delivered to the right and left hippocampus once every 24 h.

Results: All animals developed a stage 5 convulsion with a mean of 28.1 ± 3.3 (mean ± SEM) stimulations. The right and left hippocampus received 14.8 ± 1.7 and 14.6 ± 1.6 stimulations, respectively. Behavioral stages induced by stimulation of the right or left hippocampus evolved to generalized seizures along a similar course. Kindling antagonism was not observed. The two sides showed similar increases in AD duration, and similar chronologic changes in interictal discharge (IID) frequency. Simple A-type IID and complex types of IID appeared at higher rates, whereas simple B-type IID remained at a relatively low level.

Conclusions: The present AK procedure did not induce kindling antagonism, but it induced progression of kindling manifestations. The origin of simple B-type IID is known to be in the contralateral side, and its intracellular counterpart corresponds to a sequence of small depolarization followed by large hyperpolarization, suggesting that plastic changes in the feed-forward inhibitory system play an important role in hippocampal kindling.

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Volume44, Issue3

March 2003

Pages 292-298

Epileptogenesis Induced by Alternate-site Kindling in Bilateral Hippocampi

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Epileptogenesis Induced by Alternate-site Kindling in Bilateral Hippocampi

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