The role of GABA and excitatory amino acids in the development of the leptazol-induced epileptogenic EEG.

摘要: Abstract The developing epileptogenic electroencephalogram (EEG), seen during the slow intravenous infusion of leptazol, is sensitive to various anticonvulsant drugs, particularly those known augment function γ-aminobutyric acid (GABA), such as clonazepam and sodium valproate, which specifically prolong earlier wave-like (pre-spiking) phases. Thus, whilst antagonism GABA may be responsible for spiking, early phases due released in cortex a feedback control delay spiking. Intravenous antagonists, bicuculline picrotoxin, produced EEG with spiking first abnormal feature noted no phase, like that leptazol. Cortical superfusion enhanced kand prolonged reduced it. picrotoxin or larger concentrations but activity. When leptazol were superfused together they activity similar infusions Of excitatory amino only active at receptors N-methyl- d -aspartate (NMDA) influenced changes induced by It suggested produces waves stimulating subcortical pathways release occurs further stimulated acids.