Amygdaloid kindling was induced by daily electrical stimulation in the left amygdala in five groups of cats: a chronic cocaine pretreatment group; a chronic methamphetamine (MAP) pretreatment group; two treatment groups, one using pimozide and the other haloperidol during the period when kindling was being induced; and a drug-free control group. The number of left amygdaloid stimulations required for generalized convulsions was significantly greater in the two chronic pretreatment groups and significantly less in the two treatment groups, compared to the control group. All animals in the chronic cocaine and MAP pretreatment groups showed hemiconvulsions instead of symmetrical generalized convulsions and lateralized interictal discharges in the stimulated hemisphere. In rekindling to the right amygdala, seizure development was significantly suppressed compared to the control group. In the two chronic pretreatment groups, chronic administration of cocaine or MAP was followed by enhancement of behavioral responses to cocaine, MAP, and apomorphine. The association of such "sensitization" with impairment of the kindling process suggests that dopamine receptor sensitivity is an important factor in this form of epileptogenesis.

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