Electroconvulsive seizures inhibit amygdala kindling: implications for mechanisms of action in affective illness.
Amygdala kindling, the progressive development of seizures following repeated electrical stimulation, has been used as a model of epileptogenesis, neural memory, and the development of behavioral alterations. In an attempt to interfere with the kindling process, electroconvulsive seizures (ECS) were administered 6 h prior to or immediately after once-daily amygdala stimulation. ECS compared with sham ECS 6 h prior to kindling profoundly inhibited the development of amygdala-kindled seizures, while ECS immediately after the afterdischarge (AD) were not effective. In a second study, seven daily ECS, but not a single ECS followed by a 6-day delay, markedly suppressed established amygdala-kindled seizures compared with sham ECS controls. The generalized seizures of ECS thus appear to be paradoxically anticonvulsant to limbic seizures. Carbamazepine, a potent anticonvulsant for temporal lobe and limbic seizures in animals and man, inhibits amygdala-kindled seizures and is effective in the treatment of manic-depressive illness. The current findings suggest the possibility that the efficacy of ECS in affective illness may be, in part, related to its limbic antikindling and anticonvulsant effects.
D000679:Amygdala / Q000502:physiology*; D000818:Animals; D001714:Bipolar Disorder / Q000503:physiopathology; D004565:Electroconvulsive Therapy; D006801:Humans; D007696:Kindling, Neurologic; D008297:Male; D051381:Rats; D012640:Seizures / Q000503:physiopathology*