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Effects of Unilateral Ventral Hippocampal Lesion on Amygdaloid Kindling in Cat

It is suggested that the prognosis of surgical treatment for intractable epilepsy depends, in part, on the existence of a secondary epileptogenic lesion in other brain structures.’ The transference phenomenon in a kindling model of epilepsy has been considered to reflect such secondary epileptogenic changes in the brain.2 It appears relevant to get some insight into the pathophysiology of the secondary epileptogenesis if a neuronal mechanism of the transference phenomenon is elucidated. Our previous study showed that the transfer of the amygdala (AM) kindling to the contralateral AM was inhibited by either an electrolytic lesion of the bilateral ventral hippocampus or destruction of the fornix of the primary site hemisphere, and suggested that the hippocampus and the fornix are involved in the transsynaptic changes essential for an emergence of secondary epileptogenesis in the contralateral AM.:’ In this study, we examined this hypothesis by a destruction of the unilateral ventral hippocampus (VH) in AM kindling of cats.