The substantia nigra is an important site for the containment of seizure generalization in the kindling model of epilepsy

• Published in: Epilepsia (Copenhagen) Vol. 28; no. 1; p. 1
• Main Authors: Morimoto, K, Goddard, G V
• Format: Journal Article
• Language: English
• Published: United States 01-01-1987
• Subjects: Amygdala - drug effects; Amygdala - physiology; Animals; Cerebral Cortex - drug effects; Cerebral Cortex - physiology; Dopamine - physiology; Dopamine Antagonists; Electric Stimulation; Functional Laterality - physiology; GABA Antagonists; gamma-Aminobutyric Acid - physiology; Haloperidol - pharmacology; Kindling, Neurologic; Male; Neural Pathways - drug effects; Neural Pathways - physiology; Neurons - drug effects; Neurons - physiology; Picrotoxin - pharmacology; Rats; Rats, Inbred Strains; Seizures - etiology; Seizures - prevention & control; Substantia Nigra - drug effects; Substantia Nigra - physiology
• ISSN: 0013-9580
• DOI: 10.1111/j.1528-1157.1987.tb03613.x

To investigate the role of the substantia nigra (SN) in kindling, electrical stimulation of the SN was delivered at various times before or after stimulation of the amygdala (AM) or pyriform cortex during or after kindling in rats. The results were as follows: Ipsilateral SN stimulation delivered prior to each AM kindling stimulation for 14 days significantly retarded the appearance of Stage 4 and 5 seizures and shortened the afterdischarge (AD) duration. Bilateral SN prestimulation blocked seizure generalization in some AM- or pyriform cortex-kindled animals, prolonged the latency to bilateral forelimb clonus in others, and shortened the AD duration of the kindled seizure in a current intensity-dependent fashion. These effects were only partially antagonized by haloperidol, but were completely abolished by picrotoxin. The picrotoxin alone significantly reduced the latency. Almost no effect was found when the SN stimulation was delivered after the onset of bilateral forelimb clonus. We conclude that the SN might be an important mediator of the early aspects of seizure generalization from limbic epileptic foci. The relative involvements of GABAergic gamma-aminobutyric acid and dopaminergic systems of the SN in this inhibitory function are discussed.