title: Secondary epileptogenesis in frog forebrain: effect of inhibition of protein synthesis.
abstract: Secondary epileptogenesis was induced in the hippocampal cortex of the paralyzed bullfrog by means of localized, unilateral, intermittent electrical stimulation (kindling). Stimuli were designed to yield a brief but definite after-discharge. In control animals a progressive increase in after-discharge duration occurred at the 1 degree (stimulated) site and then at the 2 degrees site (contralateral hippocampus). Spontaneous epileptiform potentials (SEP's) occurred between stimuli, eventually independently on both sides. Cycloheximide (50 mg/kg) caused 88-99% reduction in protein synthesis, measured by 14C-leucine incorporation into brain protein. Cycloheximide-treated animals revealed no evidence of progressive prolongation of after-discharge duration when subjected to the kindling procedure (p = 0.1205 X 10(-7)). SEP's were reduced in the cycloheximide-treated animals, and confined to 1 degree hemisphere (p = 0.6 X 10(-10)). Since cycloheximide did not disturb normal electrogenesis or disrupt the after-discharges, this experiment distinguishes processes dependent upon electrical events from those requiring macromolecular synthesis. Protein synthesis seems critical to the emergence of spontaneous and autonomous epileptiform behavior of neural aggregates.
mesh_terms: D000818:Animals; D001001:Anura; D001522:Behavior, Animal / Q000187:drug effects; D001921:Brain / Q000187:drug effects* / Q000378:metabolism / Q000503:physiopathology; D003513:Cycloheximide / Q000008:administration & dosage*; D005071:Evoked Potentials / Q000187:drug effects; D009419:Nerve Tissue Proteins / Q000096:biosynthesis; D012640:Seizures / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D013997:Time Factors
chemical_list: D009419:Nerve Tissue Proteins; D003513:Cycloheximide