The studies on cystatin B deficient mice: neurochemical and behavioural alterations in animal model of progressive myoclonus epilepsy of Unverricht–Lundborg type

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2007-08-21T12:06:28Z

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The study aimed to further characterize the neurochemical and behavioural phenotype of cystatin B deficient mice, which are the animal model of progressive myoclonus epilepsy of Unverricht–Lundborg type. Cystatin B deficiency provokes impairment in glutamatergic neuronal circuits and enhances tryptophan metabolism along kynurenine and serotonin pathways in the brain of mutant mice. Observed neurochemical alterations may contribute to the pathological mechanisms and might have a causal impact to the formation of neurological phenotype seen in diseased humans. Käesolevas uurimuses kirjeldatakse täpsemalt Unverricht-Lundborgi tüüpi müokloonilise epilepsia mudellooma tsüstatiin B geeni puudulikkusega hiire neurokeemilist ja käitumuslikku fenotüüpi. Leitud muutused mutantsete hiirte aju trüptofaani metabolismis ning erutus– ja pidurdusnärviringete omavahelises tasakaalus võivad mõjutada müokloonilisele epilepsiale iseloomuliku haiguspildi väljakujunemist ning selgitada patoloogilisi mehhanisme inimesel.

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