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• W2022707898 abstract "Inactivation of genes for the synaptic terminal proteins synapsin I and synapsin II leads to development of epileptic seizures in mice (Syn-DKO mice) in which no other behavioral abnormalities or any gross anatomical brain deformities have been reported. In humans, mutated synapsin I is associated with epilepsy. Thus, the Syn-DKO mouse might model human seizure development. Here we describe a neuroethological analysis of behavioral elements and relationships between these elements during seizures in Syn-DKO mice. The seizure elements belong to one of three clusters each characterized by specific patterns of activity: truncus-dominated elements, myoclonic elements, and running-fit activity. The first two clusters, constituting the majority of seizural activity, evolve quite differently during ongoing seizure activity. Whereas truncus-dominated elements unfold in a strict sequence, the myoclonic elements wax and wane more independently, once myoclonic activity has started. These differences may point to neurobiological mechanisms relevant to both rodent and human epilepsies." @default.
• W2022707898 created "2016-06-24" @default.
• W2022707898 creator A5047491013 @default.
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• W2022707898 date "2009-04-01" @default.
• W2022707898 modified "2023-09-25" @default.
• W2022707898 title "Seizure elements and seizure element transitions during tonic–clonic seizure activity in the synapsin I/II double knockout mouse: A neuroethological description" @default.
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• W2022707898 doi "https://doi.org/10.1016/j.yebeh.2009.02.021" @default.
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