Lasting Secondary Antiepileptogenesis Induced by Cingulate Kindling

Abstract

Summary:Purpose: To test the validity of a hypothesis that kindling-induced enduring kindling inhibition of the homotopic secondary site is not a primate species-specific effect but occurs also in feline species.Methods: Five mature male cats were kindled at the anterior (AC) and posterior (PC) cingulate cortex followed by secondarysite kindling and primary-site retest.Results: Kindling was characterized by a marked seizure-stage instability and a progressive afterdischarge threshold elevation in all the animals. A protracted nonconvulsive seizure stage was followed by convulsive evolution and rapid generalization. At the secondary site, positive transfer effect was absent, and kindling did not occur. Primary-site retest activated kindled seizure within three stimulations. Recurrent spontaneous seizures, identical to the primary-site kindled seizure, occurred in two AC-kindled animals. Subsequent to this, a markedly elevated afterdischarge threshold also was found at some distant cortical and subcortical sites, to which the afterdischarge propagated. Kindling of the amygdala ipsilateral to the kindled AC or PC was tardy, with no positive transfer effect. However, it was associated with afterdischage threshold reduction.Conclusions: Cingulate kindling-induced enduring kindling inhibition at a homotopic secondary site is not a primate speciesspecific effect and occurs also in feline species. It is not limited to a homotopic site and represents a lasting secondary antiepileptogenesis, presumably due to enhanced intrinsic inhibitory mechanism(s) available to the mammalian brain. A selective afterdischarge threshold elevation concurrently observed is suspected to be a feline species-specific effect.

Anterior Cingulate epilepsy: mechanisms and modulation

“…This antiepileptic effect is not specific to primates because it was also shown to occur in cats. They also showed that the antiepileptic effect was not confined to the contralateral homotopic site, and the antiepileptic effect is presumably attributable to an enhanced intrinsic inhibitory mechanism in the mammalian brain (Wada and Hirayasu, 2004). …”