RESUMEN
Amygdala kindling stimulation produced significant changes in plasma zinc levels in cats otherwise unaffected by zinc loading or deprivation. While a normal diet had no effect, moderate zinc loading was accompanied by a marked increase in plasma zinc during kindling. Conversely, plasma zinc sharply declined in animals fed a zinc-deficient diet. Corresponding differences were obtained in the development of generalized seizures with kindling such that loading delayed and deprivation accelerated this process.
Asunto(s)
Dieta , Absorción Intestinal , Excitación Neurológica , Zinc/metabolismo , Animales , Gatos , Zinc/sangreRESUMEN
Sleep deprivation enhances seizure susceptibility in experimental and human epilepsies. Because sleep abnormalities are also common in these populations, a possible explanation for this close association is that sleep deprivation activates seizures by enhancing existing sleep disturbances. The present experiment examined this hypothesis by comparing sleep-waking state percentages and the number of after-discharge-eliciting stimulations required to induce generalized tonic-clonic convulsions with the amygdala kindling model of epilepsy in 3 groups of cats (n = 5 each). One group consisted of experimental subjects who received bilateral lesions of the basal forebrain, a preoptic area long implicated in the generation of normal sleep state characteristics. A second group sustained unilateral lesions of the basal forebrain area. Since only bilateral destruction of this region produces sleep-waking cycle abnormalities, this group provided a lesion control. Finally, a third group had no lesion and provided a control which allowed normative assessment of sleep state patterns and seizure susceptibility in otherwise unmanipulated cats. The results were: cats without lesions showed a parallel development of seizure and sleep disorders, the latter indexed by progressive SWS and REM sleep deficits; cats with unilateral lesions showed identical trends in the development of sleep and seizure anomalies; and cats with bilateral lesions of basal forebrain displayed similar but more severe sleep disturbances than those evidenced by control subjects and also required fewer after-discharge stimulations to establish kindled convulsions.(ABSTRACT TRUNCATED AT 250 WORDS)
Asunto(s)
Excitación Neurológica , Área Preóptica/fisiología , Convulsiones/fisiopatología , Privación de Sueño/fisiología , Amígdala del Cerebelo/fisiología , Animales , Gatos , Electroencefalografía , Epilepsias Mioclónicas/fisiopatología , Convulsiones/etiología , Sueño REMRESUMEN
This study examined the effects of protein synthesis inhibitors on sleep and seizure susceptibility in amygdala-kindled cats. Six cats with stable seizure thresholds were treated with 150 mg/kg of chloramphenicol or its cogener, thiamphenicol, at 12-h intervals over a 30-h period. State pattern variables were monitored continuously during the first 18 h. At 30 h, kindled seizure thresholds were measured in terms of minimum stimulus intensities (microA) required to elicit generalized tonic clonic convulsions. All cats were exposed to both drugs, with a 1-week intertrial interval and the order of drug treatment counterbalanced. Rapid eye movement (REM) sleep was significantly attenuated after chloramphenicol but was unaffected by thiamphenicol, as previously shown. Seizure thresholds were unaltered regardless of changes in sleep state physiology. The results extend previous work showing that protein synthesis inhibitors which suppress REM sleep increase seizure susceptibility only in animals that are either highly predisposed to seizures or that display REM sleep disruption as the sole sleep deficit associated with their seizure condition.