title: Seizure elements and seizure element transitions during tonic-clonic seizure activity in the synapsin I/II double knockout mouse: a neuroethological description.
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.
authors.affiliation: Department of Physiology, Institute of Basic Medical Sciences, University of Oslo, Blindern, Oslo, Norway. lars.etholm@medisin.uio.no
authors.forename: Lars
authors.initials: L
authors.lastname: Etholm
authors.forename: Paul
authors.initials: P
authors.lastname: Heggelund
mesh_terms: D000818:Animals; D001522:Behavior, Animal; D004195:Disease Models, Animal; D004569:Electroencephalography; D005260:Female; D008297:Male; D051379:Mice; D018345:Mice, Knockout; D012640:Seizures / Q000235:genetics* / Q000503:physiopathology*; D016704:Synapsins / Q000172:deficiency*; D014743:Videotape Recording
chemical_list: D016704:Synapsins