title: Sleep disruption with basal forebrain lesions decreases latency to amygdala kindling in cats.
abstract: 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)
mesh_terms: D000679:Amygdala / Q000502:physiology; D000818:Animals; D002415:Cats; D004569:Electroencephalography; D004831:Epilepsies, Myoclonic / Q000503:physiopathology; D007696:Kindling, Neurologic; D011301:Preoptic Area / Q000502:physiology*; D012640:Seizures / Q000209:etiology / Q000503:physiopathology*; D012892:Sleep Deprivation / Q000502:physiology*; D012895:Sleep, REM