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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Sleep disruption with basal forebrain lesions decreases latency to amygdala kindling in cats.

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)[1]


  1. Sleep disruption with basal forebrain lesions decreases latency to amygdala kindling in cats. Shouse, M.N., Sterman, M.B., Hauri, P.J., Belsito, O. Electroencephalography and clinical neurophysiology. (1984) [Pubmed]
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